Frequently asked questions

No. They are alternatives, not a stack — both are incretin receptor agonists with overlapping mechanisms, so combining them adds side-effect risk without a clear benefit. People typically switch from semaglutide to tirzepatide for greater efficacy rather than taking both. To preserve lean mass, tirzepatide is sometimes paired with a GH secretagogue like ipamorelin.

Yes — like other weight-loss therapies that work through caloric deficit, a meaningful share of the weight lost is lean mass (clinical-trial estimates around a third to 40%). Resistance training and adequate protein intake (roughly 1.2–1.6 g per kg of body weight daily) are widely recommended during therapy to preserve muscle.

Inhibits NNMT (nicotinamide N-methyltransferase), an en.

Anti-inflammatory agent that helps with leptin resistance and fat partitioning. Inhibits IKKe and TBK1, two kinases involved in inflammation and energy storage. Adds metabolic resilience when combined with other fat-loss peptides.

AOD-9604 replicates the lipolytic domain of growth hormone without its anabolic or diabetogenic effects: 1. Lipolysis Stimulation: AOD-9604 activates hormone-sensitive lipase (HSL) in adipose tissue, promoting the breakdown of stored triglycerides into free fatty acids and glycerol. This occurs through a beta-3 adrenergic receptor-associated pathway.

Mimics the N-terminal end of SNAP-25, a protein involved in muscle contraction. Inhibits the release of neurotransmitters at the neuromuscular junction, reducing facial muscle tension.

BPC-157 acts through several converging pathways rather than a single receptor. It promotes angiogenesis (new blood-vessel growth via VEGF), activates the FAK-paxillin pathway that drives cell migration and wound closure, modulates the nitric-oxide system in a tissue-context-dependent way, and upregulates local growth-hormone receptors. Together these support its broad tissue-protective effects in animal models.

Synthetic gonadotropin-releasing hormone (GnRH) analog. Initially increases, then suppresses LH and FSH through receptor downregulation. In short-term pulsatile use (5-7 days), it acts as an HPTA rebooter — the initial surge of LH/FSH jumpstarts natural testosterone production before suppression occurs.

Cagrilintide mimics amylin, a hormone co-secreted with insulin after meals that controls satiety. It activates amylin receptors (calcitonin receptor plus RAMP complexes) in the brainstem and hypothalamus to increase fullness, and engages the calcitonin receptor directly (the "dual" in DACRA). It also slows gastric emptying and blunts post-meal glucagon. Engineering gives it a roughly 7-day half-life for weekly dosing.

Acts as an intracellular buffer against oxidative stress and glycation (the damaging process where sugars bind to proteins/lipids). Provides antioxidant defense at the cellular level. Supports neuroprotection and metabolic regulation.

Contains growth factors that nourish the brain. Promotes neurogenesis, inhibits apoptosis, and supports synaptic plasticity. Supports neuroprotection, synaptic repair, and reduces glial overactivation.

CJC-1295 binds GHRH receptors on pituitary somatotroph cells, activating a cAMP/protein-kinase-A cascade that triggers growth hormone synthesis and release. The released GH stimulates the liver to produce IGF-1, the main mediator of GH's effects on muscle, bone, and connective tissue. Because it prompts the body's own pulsatile GH output, it differs from injecting synthetic GH directly.

Peptide complex extracted from calf/porcine cortex. Acts as a neurotrophic factor, supporting synaptic plasticity, antioxidant defense, and cerebral blood flow. Provides neuroprotection and memory enhancement.

Vilon (KE), Livagen (KEDA), Vesugen (KED) and Epithalon all have at least named in vitro or human mechanistic studies. Crystagen does not — it has the weakest evidence base of the commonly sold Cytogens, resting on class analogy and vendor material rather than its own data.

Enhances synaptogenesis (formation of new synaptic connections) and may support BDNF signaling pathways. Promotes long-term synaptic connectivity critical for learning and memory. Stimulates neurotrophic activity and neurogenesis.

Targets thalamic and hypothalamic pathways involved in sleep regulation. Promotes delta wave activity during deep sleep stages.

Epithalon operates through several interconnected pathways: 1.

Blocks myostatin, the protein that naturally limits muscle growth. Creates hyper-anabolic microenvironment post-workout by removing the genetic ceiling on hypertrophy. Also plays a role in inflammation and fibrosis reduction.

Selectively targets senescent cells by disrupting the interaction between Foxo4 and p53 proteins. In senescent cells, Foxo4 binds p53 to prevent apoptosis, keeping damaged cells alive. Foxo4-DRI competes for this binding, freeing p53 to trigger apoptosis specifically in senescent cells.

GHK operates through multiple interconnected pathways: 1. Extracellular matrix remodeling: Activates matrix metalloproteinases (MMPs) for controlled ECM turnover while simultaneously upregulating collagen I, collagen III, elastin, and decorin synthesis (PMID: 41209547) 2. Fibroblast activation: Promotes fibroblast migration, proliferation, and differentiation; stimulates production of glycosaminoglycans (GAGs) including hyaluronic acid 3.

GHK-Cu acts as a copper-delivery and signaling molecule. It stimulates collagen and elastin production and supports tissue remodeling, and gene- expression analysis suggests it shifts the activity of a large number of human genes — upregulating DNA-repair, antioxidant, and stem-cell pathways while downregulating inflammatory ones — effects characterized largely in cell and laboratory studies.

All three raise endogenous growth hormone through the ghrelin receptor. GHRP-2 has a moderate appetite effect and can raise cortisol and prolactin. GHRP-6 is the strongest appetite stimulant. Ipamorelin is the most selective, with little effect on cortisol, prolactin, or hunger. GHRP-2 can substitute for Ipamorelin in GH stacks when a stronger ghrelin effect is acceptable.

GHRP-2 mimics ghrelin and binds the growth hormone secretagogue receptor (GHS-R1a) on the pituitary, triggering a pulse of endogenous growth hormone. Activating the ghrelin pathway also increases hunger. It is frequently paired with a GHRH analog such as CJC-1295, because combining a GHRH analog with a GHRP produces a larger, synergistic GH pulse than either alone.

All three are ghrelin-receptor secretagogues that raise endogenous growth hormone. GHRP-6 is the strongest appetite stimulant of the group. GHRP-2 also raises hunger and can elevate cortisol and prolactin. Ipamorelin is the most selective, with minimal effect on cortisol, prolactin, or appetite. Choice depends on whether appetite stimulation is wanted or avoided.

GHRP-6 mimics ghrelin and binds the growth hormone secretagogue receptor (GHS-R1a) on the pituitary and hypothalamus, prompting a pulse of endogenous growth hormone. Activating the ghrelin pathway also strongly stimulates appetite, more so than other GHRPs. It is mechanistically similar to GHRP-2 but with more pronounced hunger effects, and is often paired with a GHRH analog such as CJC-1295.

Epithalon (pineal) and Thymalin (thymus) have decades of named studies and, for the pineal/thymus pair, a controlled human mortality trial. Glandokort has none of its own — it sits in the weakest-evidence tier of the line, alongside the other organ extracts Svetinorm (liver) and Ventfort (vascular), all of which return zero PubMed records. It rides on class analogy and vendor material rather than its own data.

Synthetic GnRH that gives direct pituitary stimulation, triggering LH/FSH release. Supports the full HPTA loop: hypothalamus to pituitary to testes. Mimics physiologic LH/FSH pulses.

Mimics luteini.

Modified form of HGH that includes only the amino acid sequence (positions 176-191) responsible for lipolytic action. Selectively activates fat breakdown without the anabolic or growth effects of full HGH. Does not raise IGF-1 levels, making it a targeted fat-loss tool.

Activates AMPK, restoring energy production pathways; a specific humanin-to-PGC-1alpha link is not established in primary literature [PMID unverified — flagged 2026-06-19]. Promotes mitochondrial biogenesis and cellular energy restoration. Acts as a cytoprotective peptide, protecting cells from apoptosis and oxidative stress.

Short half-life provides locali.

Direct action on muscle tissue via IGF-1 receptor binding. Increases contractile tissue and satellite cell proliferation. Enhances recovery and growth of high-frequency-use muscles.

Ipamorelin binds the ghrelin receptor (GHS-R1a) on pituitary cells — the same receptor the hormone ghrelin uses. Activating it triggers a calcium- mediated signaling cascade that releases stored growth hormone. Unlike older secretagogues, ipamorelin does this selectively, producing a clean GH pulse without meaningfully raising cortisol or prolactin, which is its main advantage in this class.

Kisspeptin is the primary upstream activator of the reproductive hormone cascade: 1. KISS1R (GPR54) activation: Kisspeptin binds GPR54 on GnRH neurons in the hypothalamic arcuate nucleus and anteroventral periventricular nucleus.

KPV's anti-inflammatory mechanism is distinct from most peptides: 1. Nuclear NF-kB Inhibition: KPV enters the cell nucleus and directly interacts with NF-kB transcription complexes, preventing the transcription of pro-inflammatory genes (TNF-alpha, IL-1beta, IL-6, IL-8, COX-2). This is a melanocortin receptor-independent mechanism -- KPV does not need to bind MCR on the cell surface to exert its effects.

Liraglutide activates the GLP-1 receptor (GLP-1R), a class B G-protein coupled receptor expressed across multiple organ systems: 1. Pancreas: Glucose-dependent insulin secretion from beta cells (incretin effect); suppression of glucagon from alpha cells. Does not cause hypoglycemia in normoglycemia due to glucose-dependent mechanism.

Antimicrobial peptide that restores microbiome balance, suppresses fungal overgrowth, and clears bacterial overgrowth. Heals leaky gut and retrains immune tolerance. Destroys bacteria directly while modulating inflammatory response.

Synthetic analog of alpha-MSH that stimulates melanin production by binding to melanocortin-1 receptors (MC1R) in skin cells. Enhances tanning response and may reduce UV-induced skin damage through increased melanin. More selective for MC1R than Melanotan-II, which also activates MC3R/MC4R (sexual arousal pathways).

Melanotan II activates all five melanocortin receptor subtypes non-selectively. At MC1R on melanocytes it drives melanin (eumelanin) production, causing UV-independent skin darkening. At MC3R and MC4R in the hypothalamus it suppresses appetite and influences sexual arousal and erectile function. This broad, non-selective activity is also why it produces wide-ranging off-target effects.

MK-677 is a ghrelin mimetic. It binds the GHS-R1a receptor in the pituitary and hypothalamus and stimulates the pituitary to release growth hormone in a physiologic, pulsatile pattern. The downstream rise in IGF-1 (insulin-like growth factor-1) drives most of its biological effects. In human trials, 25 mg/day raised IGF-1 by roughly 40-90% and increased fat-free mass.

MOTS-c operates through a unique mitochondria-to-nucleus signaling pathway: 1. AMPK activation — MOTS-c's primary mechanism is activation of 5'-AMP-activated protein kinase (AMPK), the master metabolic sensor. AMPK activation shifts cellular metabolism toward catabolic pathways: increased glucose uptake, fatty acid oxidation, and mitochondrial biogenesis.

NAD+ participates in cellular metabolism through several critical pathways: 1. Sirtuin Activation (SIRT1-7): NAD+ is the obligate substrate for sirtuin deacetylases. Sirtuins regulate gene silencing, DNA repair, metabolic adaptation, and stress resistance.

Supports working memory and verbal fluency through modulation of glutamate receptors. Enhances BDNF and NGF expression. Provides neuroprotective effects against oxidative stress and excitotoxicity.

Boosts neurogenesis with a focus on hippocampal growth. Reduces neuroinflammation. Adds a mood-lifting neurogenic edge over time.

Neuropeptide hormone secreted by the posterior pituitary. Promotes bedtime bonding and emotional security. Activates calm-rest-digest (parasympathetic) circuitry and social safety signals.

Targets and reduces expression of p21, a key cell cycle inhibitor associated with cellular aging and senescence. May restore regenerative potential in aged tissues. Helps regenerate neural pathways lost to age or stress.

Splice variant of IGF-1 that activates satellite cells in muscle tissue. PEGylation extends its half-life for better systemic distribution compared to native MGF.

Analog of amylin, a hormone co-secreted with insulin by pancreatic beta cells. Slows gastric emptying to reduce post-meal glucose spikes. Suppresses post-meal glucagon secretion.

PT-141 acts through the melanocortin system, a neuroendocrine pathway with broad physiological roles: 1. MC3R/MC4R agonism — PT-141 binds melanocortin receptors 3 and 4 (MC3R and MC4R) in the hypothalamus, particularly in the paraventricular nucleus and medial preoptic area. These regions are central integrators of sexual motivation and arousal (PMID: 41002740).

Retatrutide engages three receptors with complementary effects. The GLP-1 and GIP arms suppress appetite, slow gastric emptying, and improve insulin response — similar to tirzepatide. The added glucagon-receptor agonism is proposed to raise energy expenditure and promote fat oxidation, including in the liver. The net effect in trials is large weight loss, though the mechanism is still being characterized.

Retinalamin acts as a tissue-specific bioregulator: its constituent peptides are taken up by retinal cells and operate epigenetically to normalize gene expression, stimulate proliferative activity of retinal pigmented epithelial cells, and support photoreceptor and ganglion cell survival. The active fractions have been shown to induce differentiation of retinal progenitor-type cells in culture.

Selank operates through multiple neurochemical and immune pathways: 1.

Semaglutide activates the GLP-1 receptor in the brain, pancreas, gut, and other tissues. In the hypothalamus it reduces hunger and increases satiety; in the pancreas it stimulates glucose-dependent insulin release (only when blood sugar is high, limiting hypoglycemia) and suppresses glucagon; and it slows gastric emptying, prolonging fullness and blunting post-meal glucose spikes.

Semax operates through several interconnected neurobiological pathways: 1. BDNF/NGF Upregulation: Semax increases expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus and cortex, promoting neuroplasticity, synaptic strengthening, and neuronal survival (PMID: 41004910). 2.

Sermorelin binds to the GHRH receptor (GHRHR) on anterior pituitary somatotroph cells. This G-protein coupled receptor activates adenylyl cyclase, increasing intracellular cAMP and activating protein kinase A (PKA). The downstream signaling cascade: 1.

SS-31 operates through a unique cardiolipin-targeted mechanism distinct from conventional antioxidants: 1. Cardiolipin binding: SS-31 binds cardiolipin (CL) on the inner mitochondrial membrane via electrostatic and hydrophobic interactions. The Dmt (2',6'-dimethyltyrosine) residue is critical for CL interaction (PMID: 41964318).

They target the same organ but differ in origin. Svetinorm is a Cytomax — a natural multi-peptide liver extract with no single defined sequence. Livagen is a Cytogen — a single synthetic tetrapeptide, Lys-Glu-Asp-Ala (KEDA). Livagen has a reported human chromatin-activation mechanism (sibling evidence, not cited here); Svetinorm has no compound-specific study of its own. The tradition is to pair the two as same-organ siblings.

TB-500 binds G-actin to regulate the cytoskeleton, enabling cells to migrate rapidly to injury sites via the PI3K/Akt pathway. It also stimulates angiogenesis (new blood-vessel formation), reduces inflammation by modulating NF-κB signaling, and has antifibrotic effects through its Ac-SDKP metabolite. Together these actions support tissue repair and regeneration across multiple tissue types.

Tesamorelin acts as a full agonist at the GHRH receptor (GHRHR) on anterior pituitary somatotrophs: 1.

It is a triple monoamine-reuptake inhibitor (dopamine + noradrenaline + serotonin). By blocking the dopamine transporter (human PET data show dose-dependent striatal occupancy up to ~80%) and the noradrenaline and serotonin transporters, it increases satiety and suppresses appetite. In diet-induced obese animals it restores blunted forebrain dopamine and silences feeding-promoting GABAergic neurons in the lateral hypothalamus. A smaller part of the effect comes from increased nighttime energy expenditure and fat oxidation.

Restores thymus function and supports immune cell education. Targets thymus output and lymphocyte maturation. Modulates immune overactivation and neuroinflammatory markers.

Ta1 operates through multiple immunomodulatory pathways: 1. TLR Signaling: Activates Toll-like receptor 9 (TLR9) on dendritic cells and macrophages, stimulating MyD88-dependent signaling cascades that upregulate MHC class I expression and antigen presentation (PMID: 41887933). 2.

Tirzepatide simultaneously activates the GLP-1 and GIP receptors. The GLP-1 arm suppresses appetite, slows gastric emptying, and improves glucose-dependent insulin secretion; the GIP arm adds further insulin and appetite-regulating effects and may improve how fat tissue handles nutrients. The dual action is thought to explain its greater weight and glucose effects relative to GLP-1-only agonists.

GnRH agonist that desensiti.

Anti-inflammatory: Suppresses NFkB-mediated production of TNF-alpha, IL-6, IL-12; shifts Th1/Th17 -> Th2/Treg balance; inhibits macrophage activation; promotes regulatory T cell differentiation (PMID: 41912527); Vasodilation: Relaxes pulmonary and systemic vascular smooth muscle via cAMP-mediated mechanisms. This is the basis for PAH orphan drug investigation; Neuroprotection: Promotes neuronal survival, reduces neuroinflammation, modulates synaptic plasticity. VIP is co-released with acetylcholine in parasympathetic neurons; Gut function: Stimulates water and electrolyte secretion in intestinal epithelium; relaxes GI smooth muscle; modulates gut motility and mucosal immunity.

In a Phase 2 trial published in 2023, retatrutide produced up to 24.2% mean body-weight loss at 48 weeks at the highest dose in adults with obesity (PMID 37366315) — among the largest reductions reported for a single agent. These are Phase 2 results; Phase 3 trials (Eli Lilly's TRIUMPH program) are ongoing and will determine confirmed efficacy and safety.

In the STEP 1 Phase 3 trial of 1,961 adults with overweight or obesity, semaglutide 2.4 mg weekly produced 14.9% mean body-weight loss versus 2.4% on placebo over 68 weeks (PMID 33567185). Separately, the SELECT trial in adults with cardiovascular disease but without diabetes showed a 20% reduction in major cardiovascular events (PMID 37952131).

In the SURMOUNT-1 Phase 3 trial, tirzepatide 15 mg weekly produced 22.5% mean body-weight loss in adults without diabetes (PMID 35658024). In the head-to-head SURPASS-2 diabetes trial, tirzepatide lowered HbA1c and body weight more than semaglutide 1 mg (PMID 34170647). It is generally the higher-efficacy option, though direct weight-loss trial designs differ.

Oral: 10-20 mg/day (most common biohacker dose); 50-100 mg/day in some research protocols; Cycle: 4-6 weeks on; Route: Oral. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 100-200 mg orally in the morning; Route: Oral; Note: Often used as adjunct in fasted-state protocols. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research protocols use 250–500 mcg, 1x daily, cycles of 12-20 weeks. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: Applied topically at 5-10% concentration, 1-2 times daily; Route: Topical (creams, serums); Note: Works best as part of a broader skincare regimen. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research-community protocols use 250–500 mcg once or twice daily, in cycles of 4–12 weeks. For local injuries it is injected subcutaneously near the site; for gut-focused use it is taken orally or injected in the abdomen. These are community-reported figures, not trial-validated doses or medical advice — consult a clinician.

Standard: 20 mcg/day for no more than 5-7 days; Route: SubQ injection or nasal spray; Critical: Short-term use ONLY — longer use causes suppression. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

In trials cagrilintide is given subcutaneously once weekly, titrated slowly (about every four weeks) to a 2.4 mg maintenance dose — the CagriSema dose — to limit nausea; Phase 2 monotherapy tested up to 4.5 mg. There is no approved consumer dose, and only gray-market supply exists. These are research figures, not medical advice — consult a clinician.

Standard: 500-1,500 mg daily oral capsules; Pairing: Often paired with. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 5 ml IM daily or every other day (most common); Cycle: 10-20 days; up to 30 days for TBI; Maintenance: 5 ml IM 2x/week; Route: Intramuscular (IM) injection; IV also used clinically. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research protocols use 100–300 mcg of the no-DAC form, one to three times daily (often before bed), in 8–12 week cycles; the DAC form is dosed roughly 1–2 mg once or twice weekly. It is injected subcutaneously on an empty stomach and frequently combined with Ipamorelin. These figures reflect research protocols, not medical advice — consult a clinician.

Standard: 10 mg IM daily for 10 days; Repeat: Every 3-6 months; Route: Intramuscular (IM) injection. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Practitioner protocols use short pulsed courses of about 10–20 mg per cycle for 10–20 days, repeated two to three times a year, subcutaneously or orally. No controlled dosing study exists for Crystagen specifically.

Oral: 4-8 mg/day (most common); 5-20 mg in research protocols; Cycle: 10 days on, 5 off; or 3-5x/week; Route: Oral (primary); SubQ also noted. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 100 mcg SubQ 30-60 minutes before bed (most common); Range: 100-500 mcg SubQ; Cycle: 4-6 weeks; can be used nightly for 3-5 days post-shift change; Route: SubQ injection; intranasal also noted. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research protocols use 5000–10000 mcg, 1x daily, cycles of 10-20 days, 2-3x per year. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 100 mcg/day IM for 10-20 days (cycle carefully); Pulse: 100 mcg/day 10-day pulse monthly; Research range: 100-300 mcg SubQ 1-2x/week; Route: IM injection; Cycle: Must be cycled carefully. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Experimental: 5-20 mg intraperitoneally in animal models; No established human protocols; Route: Research only — injection in animal studies. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Serums: 0. 01-0. 1% GHK or GHK-Cu concentration; Apply 1-2x daily to clean skin; Can be combined with other active ingredients (retinoids, vitamin C, hyaluronic acid); No reconstitution needed for commercial preparations. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

The most common route is topical — over-the-counter serums at roughly 1–2% GHK-Cu, applied once or twice daily to clean skin, sometimes combined with microneedling for penetration. Injectable use for systemic anti-aging and wound healing is reported in community protocols at around 200–500 mcg daily in 4–8 week cycles. Injectable use is not medical advice.

Commonly cited research protocols use 100–300 mcg subcutaneously, two to three times daily, and it is often timed alongside a GHRH analog for synergistic growth-hormone release. Administration is by subcutaneous injection. These figures reflect research protocols, not medical advice — consult a clinician before use.

Commonly cited research protocols use 100–300 mcg subcutaneously, two to three times daily, typically before meals; lower vascular-support protocols use about 100 mcg once or twice daily. It is administered by subcutaneous injection and often combined with a GHRH analog for synergistic GH release. These figures reflect research protocols, not medical advice — consult a clinician.

Practitioner and vendor protocols use short pulsed courses of about 10–20 mg per cycle for 10–20 days, repeated two to four times a year, subcutaneously or orally. Because of its HPA-axis target, AM cortisol is the suggested monitoring marker. These are traditional Khavinson-style regimens, not trial-validated doses, and no standardized reconstitution protocol exists.

Standard: 100-200 mcg SubQ 3x/week (not daily); Pulse dosing: 100 mcg daily in some protocols; Cycle: 2-4 weeks; Route: SubQ injection. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 250-500 IU SubQ 2-3x/week; PCT: 1,000-2,000 IU for short-term post-cycle therapy; Route: SubQ injection. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 250-500 mcg SubQ 1-2x daily; Timing: Ideally on empty stomach pre-workout or before bed; Route: SubQ injection. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Mentioned as part of MOTS-c stack category; Specific dosing protocols not well established in the book; Route: Research protocols vary. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 20-40 mcg IM immediately post-training in target muscle group; Sprint-specific: 20 mcg IM post-sprint into quads/glutes; Cycle: 4-6 week blocks; Route: IM (into target muscle — must be locali. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 10-20 mcg post-workout 2-3x/week; Muscle-specific: 20-40 mcg into target muscles (biceps/forearms); Higher dose: 30-50 mcg SubQ post-workout; Cycle: 4-6 week blocks; Route: IM (local injection into target muscle), SubQ. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Community-reported protocols use roughly 200–300 mcg per dose, one to three times daily, in cycles of about 8–12 weeks, injected subcutaneously on an empty stomach. A dose before bed is common, to align with the body's natural overnight GH pulse. These are community figures, not trial- validated doses or medical advice.

**IMPORTANT: Kisspeptin is investigational. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research protocols use 200–500 mcg, 1-2x daily, cycles of 4-8 weeks. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commercial product (pre-filled pen): Victo These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Practitioner protocols use short pulsed courses of about 10–20 mg per cycle for 10–20 days, repeated up to four times a year, subcutaneously or orally. These are traditional Khavinson regimens, not trial-validated doses.

Systemic: 50-100 mcg SubQ 2-3x/week (cycle 2-3 weeks); Spot dose: 50 mcg SubQ near lesion for acne (not systemic); Gut healing: 50-100 mcg 2-3x/week (inject or oral); Range: 100-500 mcg in research settings; Route: SubQ (spot and systemic), topical. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Cycled depending on skin type and tanning response; Route: SubQ injection; Pharmaceutical version (afamelanotide) uses implant delivery. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Melanotan II is not FDA-approved, and what follows describes documented patterns of use, not a recommendation. Reported use is a 100 mcg test dose to assess tolerance, a loading phase of about 250–500 mcg daily for 2–4 weeks, then maintenance of 250–500 mcg one to two times weekly, subcutaneously. Nausea is dose-limiting. Consult a clinician.

Nearly every published human trial used 25 mg once daily, taken orally; 10 mg/day is a common lower research dose. No injection or reconstitution is needed. These figures reflect commonly cited research protocols, not trial-validated therapeutic doses or medical advice — consult a clinician.

Commonly cited research protocols use 5000–10000 mcg, 3-5x weekly, cycles of 4-8 weeks. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research protocols use 50000–500000 mcg, 1-2x weekly (SubQ) or monthly (IV), cycles of Ongoing / maintenance protocol. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 10-30 mg/day orally or sublingually; Note: For advanced users; still considered experimental; Route: Oral, sublingual. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 20-40 mg oral daily; Cycle: 4-6 weeks; Microdose: 2-4 mg before therapy sessions; Route: Oral. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Intranasal: 5-20 IU 1-2x/day (most common); 10-50 IU depending on use case; SubQ: 5-20 IU as needed; Pre-intimacy: 10-20 IU intranasal; Pre-social: 10 IU intranasal before stressful meetings; Route: Intranasal (primary), SubQ. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 250 mcg/day (advanced users); Route: SubQ injection; Note: Still experimental — for advanced biohackers only. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Standard: 200 mcg post-PT session to target muscle; 200-400 mcg SubQ post-workout; Frequency: 2-4x/week; Route: SubQ injection, local IM to target muscle. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Practitioner protocols use short pulsed courses of about 5–10 mg per cycle for 10–20 days, repeated two to three times a year, by subcutaneous, intranasal or oral routes. These are traditional Khavinson regimens, not trial-validated doses.

Standard: 15-120 mcg SubQ before meals, titrated individually; Route: SubQ injection; Note: Nausea is common during initiation -- start low and titrate up. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research protocols use 500–2000 mcg, As needed (45 min before activity, max 1 dose/24 hrs), cycles of As needed, max 8 doses/month per FDA labeling. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Retatrutide is not FDA-approved and is not available as a compounded or prescription product, so there is no validated clinical dose. The Phase 2 protocol titrated from 1 mg weekly upward over roughly 24 weeks toward 8–12 mg. Material sold by research-peptide vendors is not quality-assured. No retatrutide dosing should be considered medical advice.

Clinical protocols from published Russian literature reconstitute a 5 mg vial and give it by parabulbar (sub-Tenon) or intramuscular injection in short 10-day courses, sometimes repeated 1–2× per year. It is not used orally. These figures reflect research protocols only — consult a clinician before use.

Standard dose: 200-400 mcg/day intranasal; Spray delivery: ~75-100 mcg per spray (0. 05-0. 07 mL of 1. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

For weight management, semaglutide is titrated slowly to limit nausea: 0.25 mg weekly for weeks 1–4, then stepping up roughly every four weeks through 0.5, 1.0, and 1.7 mg to a 2.4 mg maintenance dose. It is injected subcutaneously once weekly. Dosing should be set by a prescribing clinician, not self-directed.

Standard dose: 200-600 mcg/day intranasal; Spray delivery: Most nasal spray bottles deliver ~100 mcg per spray (0. 1 mL of 1 mg/mL); Protocol: 1-3 sprays per nostril, 1-2x daily; Cycle: 2-4 weeks on, 2 weeks off to prevent tolerance; Enhanced variant: N-Acetyl Semax Amidate (NASA) -- more potent, longer-lasting, often dosed at 100-300 mcg/day; Clear nasal passages before administration; Tilt head slightly forward, spray into each nostril; Avoid blowing nose for 10-15 minutes after application; Morning dosing preferred (stimulating effect). These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Reconstitution: Typical vial: 2 mg or 5 mg lyophili These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Reconstitution: Typical vial: 5 mg lyophili These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Practitioner and vendor protocols use short pulsed courses of about 10–20 mg per cycle for 10–20 days, repeated up to four times a year, by subcutaneous injection or orally. These are traditional Khavinson-style regimens, not trial-validated doses, and no standardized per-lot reconstitution protocol is published for this complex.

Commonly cited research protocols use a loading phase of about 2–5 mg twice weekly for 4–6 weeks, followed by roughly 2 mg once weekly for maintenance. Because TB-500 is systemic, it can be injected subcutaneously anywhere and does not require site-specific dosing like BPC-157. These figures reflect research protocols, not medical advice — consult a clinician.

Pre-mixed solution, 2 mg/vial, ready to inject; Store refrigerated at 2-8C; Single-use vials; Typical vial: 2 mg lyophili. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

In clinical trials the effective obesity dose was 0.5 mg once daily orally; 0.25 mg was milder and 1.0 mg added little extra weight loss but more side effects. Its half-life is extremely long (about 9 days), so the drug accumulates over weeks. These are research-derived figures, not validated medical dosing — there is no FDA-approved dose because tesofensine is not approved. Consult a clinician.

Standard: 10 mg/day for 5-10 days (most common cycle); Maintenance: 10 mg/day for 5 days/month; monthly pulse dosing; Low-dose: 1 mg 2-3x/week; Route: SubQ injection; Cycling: Short 10-20 day cycles; repeat quarterly or seasonally. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Commonly cited research protocols use 1500–3000 mcg, 2-3x weekly, cycles of 4-12 weeks. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

Tirzepatide is titrated slowly to reduce gastrointestinal side effects: 2.5 mg weekly for weeks 1–4, then increasing about every four weeks through 5, 7.5, 10, and 12.5 mg toward a maximum 15 mg maintenance dose. It is injected subcutaneously once weekly. The titration should be managed by a prescribing clinician.

HPTA restart: Single dose or very short course (similar to Buserelin protocol); Medical use: 3. 75-11. 25 mg IM every 1-3 months; Route: IM injection; Critical: Short-term use only for biohacking purposes. These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

They target the same organ — the vascular wall — but differ in origin. Ventfort is a natural organ-extract complex (Cytomax) with no single sequence; Vesugen is a lab-synthesized tripeptide (Lys-Glu-Asp / KED) with a known sequence. The bioregulator tradition pairs a Cytomax with its same-organ Cytogen. Vesugen at least has named in-vitro vascular studies; Ventfort has none of its own, so its evidence base is thinner.

Practitioner and vendor protocols use short pulsed courses of about 10–20 mg per cycle for 10–20 days, repeated two to four times a year, orally or subcutaneously. These are traditional Khavinson-style regimens, not trial-validated doses — no Ventfort-specific dosing study exists, and there is no standardized reconstitution protocol for this line.

Practitioner protocols use short pulsed courses of about 10–20 mg per cycle for 10–20 days, repeated two to four times a year, subcutaneously or orally. These are traditional Khavinson regimens, not trial-validated doses.

Practitioner protocols use short pulsed courses of roughly 10–20 mg per cycle for 10–20 days, repeated two to four times a year, by subcutaneous injection or orally/sublingually. These are traditional Khavinson-style regimens, not doses validated in controlled human trials.

Intranasal (CIRS protocol): Typical vial: 5 mg lyophili These figures reflect commonly cited research protocols, not medical advice — consult a clinician.

5-Amino-1MQ is a research-only compound and is not FDA-approved. Research-only compound — not FDA-approved for human use; Available through research chemical suppliers; Not yet in clinical trials for general metabolic use.

Amlexanox is FDA-approved. FDA-approved for aphthous ulcers (canker sores); Off-label use in metabolic protocols; Available via prescription.

US FDA: Not approved as a drug. GRAS status for food ingredient (2013).

Argireline is not FDA-approved. Not FDA-approved as a drug; Available as a cosmetic ingredient in skincare products; Widely available over-the-counter in anti-aging serums.

BPC-157 is not FDA-approved for any use and is sold as a research chemical; its compounding-pharmacy status under the FDA 503A framework has shifted and should be verified as current. It is not a DEA-scheduled substance. WADA prohibits it under category S0, so competitive athletes who use it will test positive.

Human safety data is limited to anecdotal reports; there are no controlled human safety trials. Community-reported side effects are mild — injection- site irritation, occasional transient nausea, rare headache or fatigue. Because BPC-157 promotes blood-vessel growth, it is precautionarily avoided in active cancer, and in pregnancy, breastfeeding, and children due to absent safety data.

Buserelin is FDA-approved. FDA-approved for prostate cancer, endometriosis, and IVF protocols; Off-label use for HPTA restart in biohacking; Requires medical supervision.

No. Cagrilintide is not FDA-approved in any form, and stand-alone cagrilintide was never submitted for approval. Novo Nordisk filed the CagriSema NDA on December 18, 2025, with an FDA decision expected around late 2026. It is not eligible for pharmacy compounding, and only gray-market research-chemical supply exists, which carries purity and dosing-accuracy risks.

Carnosine is not FDA-approved. Available as dietary supplement (not FDA-approved as a drug); Widely available over-the-counter; Well-studied with extensive safety data.

Cerebrolysin is not FDA-approved. Not FDA-approved in the United States; Widely studied and used internationally — approved in many countries outside the US; Approved in Russia and Eastern Europe for clinical use; Available through international pharmacies and research suppliers.

No. CJC-1295 is not FDA-approved. It sits in Category 2 of the FDA's bulk drug substance evaluation for 503A compounding pharmacies, meaning it is under active review. WADA prohibits it under category S2 (peptide hormones and growth factors), so competitive athletes cannot use it. It is not a DEA-controlled substance.

Cortexin is not FDA-approved. Not FDA-approved in the United States; Widely used in Russia and Eastern Europe; Available through international pharmacies.

No. Crystagen is not FDA-approved and is sold only as a research chemical. Given the absence of compound-specific data, immune claims should be treated with particular caution.

Dihexa is a research-only compound and is not FDA-approved. Research compound — not FDA-approved for human use; Not approved in any jurisdiction for clinical use; Available through research chemical suppliers.

DSIP is a research-only compound and is not FDA-approved. Research-only — not FDA-approved for human use; Available through research chemical suppliers; Not widely available in pharmaceutical-grade formulations.

US FDA: Not approved. No clinical trials registered.

Follistatin 344 is a research-only compound and is not FDA-approved. Research-only — not FDA-approved for human use; Banned in competitive sports; Available through research chemical suppliers.

FOXO4-DRI is a research-only compound and is not FDA-approved. Research-only — no human protocols established; Experimental senolytic compound; Not available through standard suppliers.

FDA: Not approved as a drug. Not regulated as a drug when used in cosmetic formulations.

GHK-Cu is not FDA-approved as a drug, but it is widely sold over the counter in cosmetic and skincare formulations, which are regulated as cosmetics rather than medicines. Injectable GHK-Cu is NOT compoundable as of June 2026 — non-injectable GHK-Cu was removed from Category 1 and injectable GHK-Cu from Category 2 in April 2026 (pending PCAC review by February 2027). It is not prohibited by WADA and is not DEA-scheduled.

Topical GHK-Cu is generally well tolerated; reported effects are mild and local, such as transient skin irritation or redness, and overuse of copper products can theoretically cause sensitivity. Injectable use lacks controlled human safety data. As with other peptides, pregnancy and breastfeeding are precautionary exclusions due to absent data.

No. GHRP-2 is a research-only compound and is not FDA-approved for human use. It is available through research-chemical suppliers and is banned in competitive sports. Because it is unapproved, purity and dosing accuracy are not guaranteed, and it should not be regarded as a clinician-validated treatment.

No. GHRP-6 is a research-only compound and is not FDA-approved for human use. It is available through research-chemical suppliers and is banned in competitive sports. Because it is unapproved, product purity and dosing accuracy are not guaranteed, and it should not be treated as a clinician-validated therapy.

No. Glandokort is not FDA-approved and is sold only as a research chemical. It is positioned within the Russian bioregulator tradition. It is not listed by WADA and not scheduled by the DEA. Given the absence of compound-specific data, its cortisol and adrenal claims should be treated with particular caution.

It should not be combined with prescription corticosteroids without physician supervision. Glandokort is marketed to influence the HPA (stress-hormone) axis, so layering it onto exogenous steroid therapy could in principle compound or confound adrenal effects. Given the complete absence of controlled data, anyone with diagnosed adrenal disease (Addison's, Cushing's) or on steroids should defer to a clinician.

Gonadorelin is FDA-approved. FDA-approved diagnostic agent; Used off-label for hormone optimi.

HCG is FDA-approved. FDA-approved for fertility and hypogonadism; Available via prescription; Off-label use common in TRT and hormone optimi.

HGH Fragment 176-191 is a research-only compound and is not FDA-approved. Research-only — not FDA-approved for human use; Available through research chemical suppliers; Banned in competitive sports.

Humanin is a research-only compound and is not FDA-approved. Research-only — not FDA-approved; Early-stage research compound; Not widely available commercially.

IGF-1 DES is a research-only compound and is not FDA-approved. Research-only — not FDA-approved for human use; Banned in competitive sports; Available through research chemical suppliers.

IGF-1 LR3 is a research-only compound and is not FDA-approved. Research-only — not FDA-approved for human use; Banned in competitive sports; Available through research chemical suppliers.

Ipamorelin is not FDA-approved for any indication and is sold as a research chemical; it has been under evaluation in the FDA 503A compounding framework. Critically for athletes, WADA prohibits it under category S2 (peptide hormones and growth factors), so its use will cause a positive doping test. It is not DEA-scheduled.

There is no long-term controlled human safety data. Community-reported side effects are usually mild — injection-site reactions, transient headache, flushing, or water retention. Because it stimulates the GH axis, caution is advised with diabetes, and it is precautionarily avoided in active cancer, pregnancy, and breastfeeding. Eating fat near dosing can blunt the GH pulse.

FDA: Not approved. Multiple active INDs for reproductive medicine applications.

US FDA: Not approved. No clinical trials registered for KPV specifically; FDA 503A: Not on the compounding bulk drug substance list.

FDA: Approved -- Victo.

Livagen is not FDA-approved and is sold only as a research chemical. While it is marketed for liver support and is generally reported as well tolerated, controlled human safety and efficacy data do not exist. Anyone with liver disease should be managed by a physician rather than relying on an unproven peptide.

LL-37 is a research-only compound and is not FDA-approved. Research-only — not FDA-approved for human use; Endogenous antimicrobial peptide (naturally occurring); Available through research chemical suppliers.

Melanotan I is FDA-approved. FDA-approved as afamelanotide (Scenesse) for EPP treatment; Off-label use for tanning; Prescription required for pharmaceutical form.

No. Melanotan II has never been FDA-approved; the FDA has issued import alerts and public warnings, and Australia's TGA and EU regulators warn against it. It is not eligible for pharmacy compounding and is marketed only as a "research chemical." WADA prohibits it at all times under category S2. Its FDA-approved selective derivative is PT-141 (bremelanotide).

Safety is a significant concern and no long-term studies exist. Very common effects include nausea, facial flushing, fatigue, and spontaneous erections; existing moles may darken and new ones appear. Because it hyperactivates melanocytes, there is a mechanistically plausible melanoma concern, with documented case reports. Illicit products also show highly variable purity. Avoid with any melanoma history or atypical moles.

No. MK-677 is not FDA-approved for any indication; development for sarcopenia and frailty was discontinued. It is sold only as a research chemical. It is technically not a peptide (it is a non-peptide peptidomimetic) but is commonly grouped with peptides. It is prohibited in sport at all times by WADA (category S2, growth hormone secretagogues).

FDA: Not approved. Not currently listed in 503A categories.

US FDA: Not approved as a drug. NAD+ available through compounding pharmacies and IV clinics.

Noopept is not FDA-approved. Not FDA-approved in the United States; Available as a supplement in some countries; Approved in Russia for cognitive enhancement; Available through nootropic and research suppliers.

NSI-189 is a research-only compound and is not FDA-approved. Research-only — not FDA-approved; Was in clinical trials for depression; Available through research chemical suppliers.

Oxytocin is FDA-approved. FDA-approved for obstetric use (Pitocin); Off-label for mood, social bonding, and intimacy support; Available via prescription in intranasal and injectable forms.

P21 is a research-only compound and is not FDA-approved. Research-only — not FDA-approved; Preclinical stage — no established human protocols; Available through select research suppliers.

PEG-MGF is a research-only compound and is not FDA-approved. Research-only — not FDA-approved for human use; Available through research chemical suppliers; Banned in competitive sports.

No. Pinealon is not FDA-approved and is sold only as a research chemical. It is used within Russian bioregulatory/neurology practice. It is not prohibited by WADA. Cognitive and neuroprotective claims are not validated by controlled human trials.

Pramlintide is FDA-approved. FDA-approved for adjunct use with insulin in type 1 and type 2 diabetes; Available via prescription (marketed as Symlin); Medical supervision required.

FDA: Approved — Vyleesi (bremelanotide injection, 1.

No. Retatrutide is an investigational compound in Phase 3 trials and is not FDA-approved or otherwise authorized for clinical use. It is sold only as a research chemical, with variable purity and authenticity. As a non-approved substance it falls under WADA's S0 category. It is not a legally marketed medicine in any jurisdiction.

No. Retinalamin is not FDA-approved. It is used clinically in Russia and Eastern Europe and is available through international bioregulator suppliers. It does not have regulatory approval in the US, EU, or UK.

No. All three are Khavinson-developed polypeptide bioregulators, but they target different tissues. Retinalamin is a retina-specific extract. Pinealon targets the pineal gland/CNS; Epithalon (AEDG tetrapeptide) is derived from the pineal gland and has separate retinal research — the two are distinct compounds with different source tissues and peptide sequences.

US FDA: Not approved. Not available by prescription in the US; Russia: Approved for GAD and neurasthenia since 2009; FDA 503A: Not on the compounding bulk drug substance list; WADA: Not prohibited; DEA: Not scheduled.

Yes. Semaglutide is FDA-approved as Ozempic (2017) and Rybelsus (2019) for type 2 diabetes and as Wegovy (2021) for weight management, and is approved in 100+ countries. WADA does not prohibit it, so athletes may use it with a valid prescription. Compounded semaglutide exists but its legal status is contested and evolving.

US FDA: Not approved. Not available by prescription.

FDA: Previously approved (Geref Diagnostic, Serono). Voluntarily withdrawn 2008.

FDA: Approved as FORZINITY (elamipretide), accelerated approval 2025-09-19, for Barth syndrome in patients >=30 kg. All other (non-Barth) uses remain investigational.

No. Svetinorm is not FDA-approved and is sold only as a research chemical. It is used within Russian hepatology/bioregulatory practice and is generally reported as well tolerated, but controlled human safety and efficacy data do not exist. Anyone with liver disease should be managed by a physician rather than relying on an unproven peptide.

No. TB-500 is not FDA-approved. It is classified as Category 2 under the FDA's bulk drug substance evaluation for 503A compounding pharmacies, meaning it is under review and may be reclassified. WADA has prohibited it under category S0 (non-approved substances) since 2011, so athletes cannot use it. It is not a DEA-controlled substance.

FDA: Approved (Egrifta, 2010; Egrifta SV reformulation, 2019) for reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. Marketed by Theratechnologies; 503A/503B: Available via compounding pharmacies for off-label use under prescriber supervision; WADA: Prohibited at all times under S2 (Peptide Hormones, Growth Factors, Related Substances, and Mimetics); DEA: Not a controlled substance; International: Approved in the US; Health Canada approval for HIV lipodystrophy.

No. Tesofensine is not FDA-approved. It reached Phase II trials for obesity with strong results but a Phase III program was never completed in the US or EU, and the pivotal Lancet trial later received an Expression of Concern over under-reported adverse events. It is sold only as a research chemical in the US. A fixed-dose tesofensine/metoprolol combination (Tesomet) has been studied for rarer indications such as hypothalamic obesity.

The most consistent objective signal is a dose-dependent rise in heart rate (about +7-8 bpm at 0.5-1.0 mg/day). Blood pressure was not significantly increased versus placebo at 0.25-0.5 mg in the obesity trial, but higher doses warrant monitoring. Common side effects were dry mouth, nausea, constipation, hard stools, diarrhea and insomnia. Because it raises dopamine, noradrenaline and serotonin, mood and sleep effects (insomnia, agitation, anxiety) are mechanistically expected, and a 2013 Lancet Expression of Concern flagged that adverse effects in the pivotal trial may have been under-reported. People with cardiovascular disease, arrhythmia, uncontrolled hypertension, anxiety disorders, or who take other serotonergic/stimulant drugs should avoid it.

This is the honest part: there is no Crystagen-specific study indexed in PubMed — no clinical trial and no named in vitro paper. Its proposed epigenetic, immune-regulating mechanism is inferred from the broader Khavinson short-peptide class (peptide regulation of gene expression, geroprotector studies). Treat Crystagen's specific claims as unproven.

This is the honest part: there is no Glandokort-specific study indexed in PubMed — no clinical trial and no named in vitro or animal paper (a PubMed search for "Glandokort" returns zero records). Its proposed epigenetic, adrenal-regulating mechanism is inferred from the broader Khavinson short-peptide/organ-extract class. Treat Glandokort's specific cortisol and adrenal claims as unproven.

This is the honest part: there is no Svetinorm-specific study indexed in PubMed — no clinical trial and no named in vitro paper. Its composition is documented only in vendor material. What exists is named Russian preclinical evidence for the liver organ-extract class: liver "cytomedins" (hepalin) stimulating hepatic tissue growth in organotypic culture (PMID: 11213728; PMID: 12096446), and a polypeptide liver complex showing hepatoprotective effects in liver-fibrosis and hepatitis models (PMID: 32362099). Svetinorm's specific claims are extrapolated from that body of work — treat them as plausible-but-unproven for this exact product.

This is the honest part: there is no Ventfort-specific study indexed in PubMed — searching "Ventfort" returns zero records, with no clinical trial, animal study, or named in vitro paper. Its vascular claims are extrapolated from (1) the broader Khavinson short-peptide bioregulator class and (2) its synthetic vascular sibling Vesugen (the KED tripeptide), whose vasoprotective effects are themselves only in-vitro and largely Russian-language. Treat Ventfort's specific claims as unproven.

Thymalin is not FDA-approved. Not FDA-approved in the United States; Widely used in Russia and Eastern Europe with decades of clinical history; Available through international pharmacies and research suppliers; Part of the Khavinson peptide bioregulator family.

US FDA: Not approved. Orphan drug designation for hepatocellular carcinoma.

Yes. Tirzepatide is FDA-approved as Mounjaro (type 2 diabetes, 2022) and Zepbound (weight management, 2023). It is not prohibited by WADA, so athletes may use it with a valid prescription. As a marketed brand-name drug it is prescription-only; gray-market "research" tirzepatide is not quality-controlled and is not the approved product.

Triptorelin is FDA-approved. FDA-approved for prostate cancer, endometriosis, and fertility protocols; Off-label use for HPTA restart; Requires prescription and medical supervision.

No. Ventfort is not FDA-approved and is sold only as a research compound. It is used within Russian bioregulatory/cardiovascular practice and is not prohibited by WADA. Because there is no compound-specific data and the core peptide-DNA mechanism is scientifically controversial, anyone with cardiovascular disease should be managed by a physician rather than self-treating with an unproven peptide.

No. Vesugen is not FDA-approved and is sold only as a research chemical. It is used in Russian cardiovascular bioregulator practice. Vascular-health claims are not supported by controlled human trials, and anyone with cardiovascular disease should be managed by a physician.

No. Vilon is not approved by the FDA, is not on the 503A compounding list, and is sold only as a research chemical. It is used within Russian bioregulatory medicine. It is not prohibited by WADA.

FDA: Not approved as a therapeutic. Orphan drug designation for pulmonary arterial hypertension (PAH).

As an investigational drug, its safety profile is still being defined. In Phase 2 the side effects were predominantly gastrointestinal — nausea, vomiting, and diarrhea — and were dose-related, consistent with the incretin drug class. Long-term safety, the impact of glucagon-receptor activation on glucose, and rarer risks remain under study in ongoing Phase 3 trials.

The most common side effects are gastrointestinal — nausea (around 40%), diarrhea, vomiting, constipation, and abdominal pain — usually worst during dose escalation. Rare serious risks include pancreatitis and gallbladder disease. It carries a boxed warning for thyroid C-cell tumors based on rodent data and is contraindicated with a personal or family history of medullary thyroid carcinoma or MEN2.

The evidence tier is mechanistic and preclinical, not large human outcome trials. As a ghrelin-receptor agonist, GHRP-2 is studied for raising endogenous growth hormone, supporting muscle growth and recovery, aiding fat metabolism, and stimulating appetite in muscle-wasting scenarios. Because robust human trial data are limited, these are research-context benefits rather than proven clinical outcomes.

The evidence tier is mechanistic and preclinical rather than large human trials. As a ghrelin-receptor agonist, GHRP-6 is studied for stimulating endogenous growth hormone, increasing appetite (useful in underweight or muscle-wasting states), supporting recovery, and aiding blood-vessel repair and nitric-oxide signaling. Human outcome data are limited, so these are research-context benefits, not proven clinical results.

Side effects are predominantly gastrointestinal and concentrated during dose titration: nausea, vomiting, diarrhea, constipation, and reduced appetite. In the Phase 3 REDEFINE 1 trial, GI events occurred in about 80% on CagriSema versus 40% on placebo, but treatment discontinuation was low (around 6%). Class concerns include pancreatitis and gallbladder disease; most safety data come from the combination, not cagrilintide alone.

Reported side effects include injection-site reactions, mild water retention, tingling or numbness in the extremities, transient flushing, increased hunger, and fatigue during adaptation. Carpal-tunnel-type symptoms are associated with sustained GH/IGF-1 elevation and are more common with the DAC form. It is contraindicated in active cancer, since IGF-1 can promote tumor growth, and in pregnancy.

Reported effects include flushing, tingling, and water retention. GHRP-2 may elevate cortisol and prolactin more than the more selective Ipamorelin, so monitoring is advised with long-term use, and effects depend on pituitary function. It stimulates appetite, though generally less than GHRP-6. It is considered to act more physiologically than direct HGH injection.

Reported effects include water retention and a pronounced increase in hunger that is stronger than with other GHRPs. With long-term use, GHRP-6 can elevate cortisol and prolactin, so monitoring is advised for chronic use. As a growth-hormone secretagogue, its overall effect depends on pituitary function. Discuss risks and bloodwork with a clinician.

Documented effects include increased appetite (it is a ghrelin mimetic), fluid retention and edema, transient muscle/joint aches, lethargy, and mildly elevated prolactin after initial doses. The most important concerns are metabolic — increased fasting glucose and reduced insulin sensitivity (it can push toward insulin resistance, especially with long-term use) — and a congestive-heart-failure safety signal that ended one hip-fracture trial early. Monitor IGF-1, fasting glucose, insulin, and HbA1c.

Published data report a generally favorable safety profile, with occasional transient head rush or lightheadedness, mild injection-site reactions, and temporary fatigue during loading. A theoretical concern is tumor promotion, since TB-500 promotes cell migration and angiogenesis, so people with active cancer should exercise extreme caution. Long-term human safety data are limited.

Side effects mirror other incretin therapies and are mainly gastrointestinal — nausea, diarrhea, vomiting, and constipation — most common during dose escalation. Rarer concerns include pancreatitis and gallbladder issues, and it carries a thyroid C-cell tumor warning based on rodent studies. It is contraindicated with a personal or family history of medullary thyroid carcinoma or MEN2.

Peer-reviewed studies document use in photochemical retinal damage models (demonstrating retinoprotection), diabetic retinopathy (structural and functional monitoring studies through 2024), glaucomatous optic neuropathy (including long-term progression data), and hereditary retinal degenerations (abiotrophy/retinitis pigmentosa context). All published human work is from Russian ophthalmology centers; no Western RCTs exist.

Phase IIb Obesity Trial: Metabolic Pharmaceuticals conducted a large (>300 patient) Phase IIb RCT of oral AOD-9604 (1mg/day) for obesity. Results showed statistically significant weight loss vs placebo but the magnitude was modest (~2. 5 kg over 12 weeks).

BPC-157 has 200+ PubMed publications, but the evidence is almost entirely preclinical — rat and mouse models of tendon, gut, muscle, and nerve injury. No completed human Phase 2/3 trials are published. A 2026 Sports Medicine review concluded rigorous human safety data are scarce and favorable animal results may not translate to humans (PMID 41966639).

The evidence tier is human RCTs in top journals. In a Phase 2 monotherapy trial, cagrilintide produced dose-dependent weight loss up to about 10.8% at 26 weeks (Lau et al., Lancet 2021, PMID 34798060). In the Phase 3 REDEFINE 1 trial, CagriSema reached roughly 20–23% weight loss versus about 16% for semaglutide alone (Garvey et al., NEJM 2025, PMID 40544433). It remains investigational.

The evidence tier is early-phase human pharmacokinetics, not large outcome trials (about 28 PubMed entries). A randomized study in healthy adults found CJC-1295 with DAC produced prolonged growth hormone and IGF-1 elevation lasting several days after a single subcutaneous dose (Teichman et al., J Clin Endocrinol Metab 2006, PMID 16352683). No large trials confirm body-composition or anti-aging outcomes.

Khavinson Longevity Studies: Professor Khavinson conducted 15+ year studies on elderly patients receiving epithalamin/Epithalon. Results showed improved biomarkers of aging, restored melatonin rhythms, and trends toward reduced mortality; Pineal Function: Human studies demonstrated restoration of melatonin synthesis in elderly patients with reduced pineal function; Clinical use in Russia: Used in bioregulatory medicine protocols, primarily in geriatric patients; Limited Western clinical trials: No FDA-registered clinical trials. Evidence base is predominantly Russian; Telomere Extension in Cell Lines (2025): Dose-dependent telomere length extension demonstrated in normal human epithelial and fibroblast cells through hTERT and telomerase upregulation.

Cosmetic studies: Multiple clinical trials of GHK-containing topical formulations demonstrate improved skin firmness, reduced wrinkles, and increased collagen density in photoaged skin; Wound healing review (PMID: 41209547): Comprehensive 2025 review confirmed GHK-based formulations (nanoparticle conjugates, hydrogels, TriHex/TriHex 2. 0) enhance fibroblast migration, ECM remodeling, collagen and elastin synthesis, and wound closure while providing antimicrobial activity; TriHex technology: Clinical dermatology products containing GHK demonstrate accelerated post-procedure healing in laser resurfacing and microneedling patients; No large-scale RCTs: Human evidence is primarily from small cosmetic trials and case series; no Phase 3 drug trials for injectable GHK; GHK accelerated wound closure in murine models by 40-60% compared to controls; Protective effects in lung fibrosis, liver fibrosis, and bone healing models; Gene expression profiling in animal tissues confirms broad genomic activation pattern; GHK-Cu-loaded hydrogels showed enhanced wound healing in diabetic mouse models (Yang X et al., Macromol Biosci, 2022. PMID: 35598070).

Foundational work by Pickart and colleagues reported that GHK can reset expression across thousands of human genes toward a healthier profile at very low concentrations (PMID 25302294) and described its role across multiple cellular pathways in skin regeneration (PMID 26236730). Most evidence is preclinical (cell and animal studies) or small-scale cosmetic trials, not large human RCTs.

The defining study by Raun and colleagues characterized ipamorelin as the first selective growth-hormone secretagogue, releasing GH without the cortisol and prolactin spikes seen with related compounds (PMID 9849822). Human development for postoperative ileus did not meet its endpoints. Most evidence is preclinical or early-stage; there are no large outcome trials for anti-aging or body-composition use.

IVF oocyte maturation trigger: KP-54 (9. 6 nmol/kg SC) successfully triggers oocyte maturation with significantly lower risk of ovarian hyperstimulation syndrome (OHSS) compared to hCG trigger. Multiple Phase 2 trials at Imperial College London (Dhillo lab) demonstrate efficacy and safety; Hypothalamic amenorrhea: KP-10 pulsatile infusion restores LH pulsatility in women with hypothalamic amenorrhea, demonstrating ability to "restart" the reproductive axis; Male hypogonadism: Single-dose KP-54 produces robust, dose-dependent LH and testosterone increases in healthy men and hypogonadal men (except those with complete GnRH deficiency); Diagnostic tool: Kisspeptin challenge test can differentiate hypothalamic from pituitary causes of hypogonadism; Sexual behavior/psychosexual effects: KP-54 administration in human fMRI studies enhances brain activation in response to sexual and romantic stimuli, suggesting roles beyond reproduction; Diabetic nephropathy (PMID: 41950743): KP-54 confers renal protection in diabetic nephropathy by ameliorating endothelial permeability through.

Limited direct human trials: No FDA-registered clinical trials for KPV specifically; Alpha-MSH Clinical Data: Parent compound alpha-MSH has clinical data in inflammatory conditions; KPV inherits the mechanistic rationale; Anecdotal/Clinical Use: Growing use in functional medicine for gut inflammation, reported improvements in IBD/IBS symptoms; Doping Review (2026): KPV identified among synthetic peptide fragments promoted for anti-inflammatory effects in sport and bodybuilding, with limited clinical evidence supporting use (PMID: 41880199); Colitis (2025-2026): KPV-based SIPPC conjugate (proKPV) achieved 3. 8-fold greater colonic accumulation than free KPV in colitis mice, with enhanced efficacy at 20-fold lower dose. Oral delivery platform with GI stability, mucus penetration, and ROS-responsive release (PMID: 41533788); Acute Lung Injury (2025-2026): Oral proKPV substantially accumulated in inflamed lungs and exhibited potent anti-inflammatory efficacy in acute lung injury mice, demonstrating applications beyond GI (PMID: 41533788); IBD Host Defense Peptide Review (2025): KPV grouped with host defense peptides having immunoregulatory mechanisms.

LEADER trial (PMID: 27295427): 9,340 patients with T2DM, 3. 8 years follow-up. Liraglutide reduced major adverse cardiovascular events (MACE) by 13% vs.

A named human study reported that Livagen activates (decondenses) chromatin in lymphocytes from older subjects, and animal work found effects on digestive-enzyme activity in the gastrointestinal tract. These are small, mostly Russian-language studies; there are no FDA-registered clinical trials, so the evidence tier is preliminary.

Formal human trials are limited; the published record is dominated by case reports and pharmacology reviews rather than safety or efficacy trials. A 2025 case report linked Melanotan II nasal spray to oral mucosal malignant melanoma in a young woman (Int J Oral Maxillofac Surg, PMID 40210573), and a 2026 case documented persistent oral mucosal pigmentation after 64 days of injections (Bonchev, Life, PMID 41752902).

MK-677 has real human RCT data. A 2-year trial in healthy older adults (Nass 2008, Annals of Internal Medicine) showed it restored GH/IGF-1 to young-adult levels and increased fat-free mass by about 1 kg, but did not improve strength or function. A 563-patient Alzheimer's trial (Sevigny 2008) raised IGF-1 ~73% but produced no cognitive benefit. It reliably raises bone-turnover markers and IGF-1, but a hip-fracture trial (Adunsky 2011) was halted early for a congestive-heart-failure safety signal. Bottom line: the biomarker effect is real, the functional/clinical benefit is largely unproven, and there are genuine metabolic and cardiac concerns.

200 PubMed publications as of April 2026. Growing rapidly — majority published after 2020. Discovery paper (Lee et al.

Aging Biomarkers: Multiple human studies show NAD+ supplementation (via NMN or NR) increases blood NAD+ levels and improves biomarkers of aging (insulin sensitivity, body composition, exercise capacity); NMN Clinical Trials: Several RCTs with NMN (250-1000mg/day oral) showing increased NAD+ metabolites, improved insulin sensitivity in overweight women, enhanced aerobic capacity in amateur runners; NR Clinical Trials (Basis/ChromaDex): NRPT (Niagen) studies showing increased blood NAD+ by ~40-90% with 300-1000mg/day NR; IV NAD+ Clinics: Growing clinical use for anti-aging, addiction recovery (BR+NAD protocol), chronic fatigue, and neuroprotection. Limited RCT data on IV administration specifically; Addiction Recovery: The BR+NAD IV protocol uses high-dose NAD+ (750-1500mg/day IV over 10 days) for opiate, alcohol, and ben.

Pinealon (EDR) has named in vitro and animal studies: it increased cell viability by suppressing free-radical levels, protected rat offspring from prenatal hyperhomocysteinemia, and stimulated serotonin expression in brain cortex cells. Some appear in international journals. There are still no FDA-registered human trials, so the evidence tier is preliminary.

114 PubMed publications as of April 2026. Unique among research peptides in having completed Phase III clinical trials and achieved FDA approval.

Russian Clinical Approval: Approved for GAD and neurasthenia.

Russian Clinical Approval: Approved for ischemic stroke (improves neurological outcomes), cognitive disorders, and peptic ulcers. Clinical trials conducted primarily in Russian institutions; Stroke Recovery: Russian clinical data show improved neurological recovery when administered within 6-12 hours of ischemic stroke onset; Cognitive Enhancement: Studies in healthy volunteers show improved attention, memory consolidation, and executive function; ADHD: Russian clinical protocols include Semax for pediatric and adult ADHD management; **Al.

Diagnostic use for GH deficiency is well-established with decades of clinical data; In GH-deficient children, sermorelin (Geref) increased growth velocity and IGF-1 levels in multiple Phase 3 trials; Studies in adults show increases in lean body mass, decreased body fat, and improved sleep architecture with 3-6 month administration; A 2026 Sports Medicine review (PMID: 41966639) noted that sermorelin is among peptides marketed for musculoskeletal recovery, but rigorous human safety data for off-label uses remain scarce; A 2026 J Clin Med review (PMID: 41598480) identified sermorelin alongside other GHRH agonists as potentially useful for preserving lean mass during weight loss, though evidence is preliminary; Robust preclinical data showing GH axis stimulation across species; Animal models demonstrate improved wound healing, cardiac function, and neuroprotection with GHRH analog administration; CJC-1295 + ipamorelin showed improved muscle function in glucocorticoid-treated mice, suggesting class-wide GHRH/GHRP effects applicable to sermorelin.

Human evidence: Barth syndrome: Phase 3 TA.

Thymosin Beta-4 is one of the most-studied peptides (over 1,000 PubMed entries), but most evidence is preclinical (animal models). It accelerated full-thickness wound closure in animal studies (Malinda et al., J Invest Dermatol 1999, PMID 10469335). The main human data come from Phase 2 corneal eye-drop trials (RGN-259). Cardiac, renal, and hair findings remain preclinical, so the human evidence tier is limited.

Meta-analysis of 5 RCTs (PMID: 41545261): Tesamorelin significantly reduced visceral adipose tissue (MD = -27. 71 cm2, P < 0. 001), trunk fat (-1.

For obesity the evidence is genuine but limited: the Phase II TIPO-1 trial (Astrup, Lancet 2008, 203 patients, 24 weeks) showed placebo-subtracted weight loss of about 4.5%, 9.2% and 10.6% at 0.25, 0.5 and 1.0 mg respectively. For its original indications the evidence is negative — randomized Parkinson's trials (early and advanced disease) and an Alzheimer's proof-of-concept trial all failed to show meaningful clinical benefit. Mechanistic support comes from human PET dopamine-transporter data and animal lateral-hypothalamus studies. No Phase III obesity trial was completed, so the overall human evidence tier is moderate, not strong.

HBV-ACLF (RCT, n=73): Open-label RCT (NCT03082885) showed Ta1 + standard therapy significantly increased 90-day transplant-free survival vs. standard therapy alone. Ta1 reduced Treg frequency and moderated late-stage hyperinflammatory response (PMID: 41887933); Gastric Cancer Neoadjuvant (Phase II, n=30): Serplulimab + SOX + thymalfasin achieved 30% pathological complete response and 56.

The KED tripeptide has been studied in vitro for vasoprotective and anti-atherosclerotic effects, modulation of vascular endothelial cell proliferation, and — more recently — neurogenesis-related gene expression. Findings are mechanistic and mostly Russian-language; there are no FDA-registered clinical trials, so the evidence tier is preliminary.

The strongest data are in vitro. The KE dipeptide has been shown to change expression of ageing-associated genes including SIRT1 and PARP1/PARP2 in human cells, and short thymic peptides of this class influence thymocyte activity and immune signalling. Human evidence is limited to Russian-language clinical reports; there are no FDA-registered trials, so the evidence tier is preliminary.

CIRS/Mold illness: The Shoemaker Protocol uses intranasal VIP (50 mcg 4x daily) as the final treatment step after correcting other biomarkers. Published case series report improvements in pulmonary artery pressure, cognitive function, fatigue, and inflammatory markers (MMP-9, TGF-beta-1, C4a, VEGF). Clinical data is primarily observational; Pulmonary arterial hypertension: VIP inhalation reduced pulmonary artery pressure and improved exercise capacity in small clinical studies.

5-Amino-1MQ is a small molecule NNMT inhibitor that preserves and boosts NAD+ levels, leading to more efficient mitochondrial energy production and fat oxidation.

Amlexanox is an anti-inflammatory compound that adds metabolic resilience by addressing leptin resistance and fat partitioning. Originally FDA-approved for treating canker sores, it has been repurposed in peptide protocols for its metabolic and anti-inflammatory properties.

AOD-9604 is a metabolic compound. Modified C-terminal fragment of human growth hormone (hGH 176-191) — stimulates lipolysis and inhibits lipogenesis without affecting IGF-1, blood glucose, or growth; beta-3 adrenergic receptor pathway modulation.

Argireline is a topical peptide that mimics the N-terminal end of SNAP-25 to inhibit neurotransmitter release at the neuromuscular junction, reducing facial tension and minimi.

The most common pairing is TB-500 (the "Wolverine stack") — BPC-157 for localized repair and TB-500 for systemic tissue remodeling. It is also combined with GHK-Cu for skin and wound healing, and is sometimes added alongside GLP-1 drugs like semaglutide or tirzepatide for its gastroprotective effect during dose titration. Stacking evidence is anecdotal.

BPC-157 (Body Protection Compound 157) is a synthetic 15-amino-acid peptide derived from a protective protein found in human gastric juice. It is studied for tissue repair — tendon, ligament, muscle, gut, and bone healing. Unusually for a peptide, it is stable in stomach acid, which is why oral dosing is viable. It is not FDA-approved.

Buserelin is a synthetic GnRH analog that initially increases, then suppresses LH and FSH through receptor downregulation. In peptide biohacking, short bursts (5-7 days) are used to reboot a suppressed HPTA axis, particularly after TRT or steroid use.

Cagrilintide (AM833) is a long-acting, once-weekly amylin analog developed by Novo Nordisk and classified as a dual amylin and calcitonin receptor agonist (DACRA). It is best known as the amylin half of CagriSema, its fixed-dose combination with semaglutide. It remains investigational and is not FDA-approved in any form. Unusually for a peptide in this space, it has a real human RCT program.

CagriSema is the fixed-dose combination of cagrilintide and semaglutide (2.4 mg each). Cagrilintide works through the amylin/calcitonin pathway while semaglutide is a GLP-1 agonist; a Phase 1b study confirmed no pharmacokinetic interaction, so their appetite effects are additive (Enebo et al., Lancet 2021, PMID 33894838). The headline 20%+ weight-loss figures belong to CagriSema, not stand-alone cagrilintide (about 10–12%).

Carnosine is a naturally occurring dipeptide composed of beta-alanine and histidine that acts as an intracellular buffer against oxidative stress and glycation -- two key contributors to aging and cellular damage. It is used for neuroprotection, metabolic regulation, and preserving muscle integrity.

Cerebrolysin is a neuropeptide blend derived from pig brain proteins containing low-molecular-weight peptides and free amino acids that cross the blood-brain barrier. It is used extensively in Europe and Asia for neurodegenerative conditions, traumatic brain injury, and stroke recovery.

CJC-1295 is a synthetic analog of growth hormone releasing hormone (GHRH). Four amino-acid substitutions make it resist DPP-IV degradation, extending its half-life versus native GHRH. It signals the anterior pituitary to release growth hormone in physiological pulses. Two forms exist: "no DAC" (Mod GRF 1-29, short-acting) and "with DAC" (albumin-bound, ~8-day half-life). It is most often paired with Ipamorelin.

Cortexin is a peptide complex derived from porcine cerebral tissue that acts as a neurotrophic factor. It is widely used in Eastern Europe for neurorehabilitation, supporting synaptic plasticity, antioxidant defense, and cerebral blood flow.

Crystagen is a synthetic short peptide sold as a thymic/immune "Cytogen" in the Khavinson bioregulator family. It is marketed for immune support and anti-inflammatory effects in ageing or immunocompromised individuals.

Dihexa is a nootropic peptide derived from angiotensin IV that enhances synaptogenesis and supports BDNF signaling pathways. It is considered one of the most potent cognitive enhancers in the peptide space, promoting long-term synaptic connectivity critical for learning and memory.

DSIP is a neuropeptide that modulates sleep-wake cycles by promoting delta wave activity during deep sleep stages.

Epithalon is a longevity compound. Activates telomerase (hTERT), potentially lengthening telomeres and extending cellular lifespan; regulates melatonin synthesis via pineal gland modulation; antioxidant properties.

Follistatin 344 binds and inhibits myostatin, a protein that limits muscle growth.

Foxo4-DRI (D-Retro-Inverso) is a novel senolytic peptide that selectively targets and neutrali.

For skin and wound healing GHK-Cu is commonly paired with BPC-157 and TB-500 (the "Glow" and "Recovery" stacks) — GHK-Cu drives collagen and tissue remodeling while the others support angiogenesis and systemic repair. It is also combined with compounds like thymosin alpha-1 in anti- inflammatory protocols. Stacking is based on practitioner reports, not controlled trials.

GHK-Cu (copper peptide) is the tripeptide glycyl-L-histidyl-L-lysine bound to a copper ion. It occurs naturally in human plasma, where levels decline with age. It is studied for skin rejuvenation, wound healing, collagen synthesis, and anti-aging gene signaling. It is most often used topically in cosmetic serums, and is not FDA-approved as a drug.

GHK is a wound healing compound. Naturally occurring tripeptide that activates wound healing genes, stimulates collagen/elastin synthesis, promotes fibroblast migration, and remodels extracellular matrix.

GHRP-2 (growth hormone releasing peptide 2) is a synthetic ghrelin-mimetic secretagogue that stimulates the body's own growth hormone release through the ghrelin receptor (GHS-R1a). It is studied for muscle growth, fat metabolism, and recovery, and is known to increase appetite. It is a research-only compound and is not FDA-approved.

GHRP-6 (growth hormone releasing peptide 6) is a synthetic peptide secretagogue that stimulates the body's own growth hormone release by activating the ghrelin receptor. Among the GHRPs it is most known for strong appetite stimulation, which has drawn research interest for muscle-wasting or underweight scenarios. It is a research-only compound and is not FDA-approved.

Glandokort is a natural adrenal-cortex polypeptide complex sold as a "Cytomax" in the Khavinson bioregulator family — a peptide mixture extracted from the adrenal tissue of young animals. It is marketed to normalise cortisol rhythm and support adrenal resilience and energy in chronic-fatigue or burnout states. It is a Cytomax (natural organ extract), not a synthetic Cytogen.

Gonadorelin is a synthetic GnRH (gonadotropin-releasing hormone) that directly stimulates the pituitary to release LH and FSH. It is used for testosterone restoration, HPTA support, and fertility preservation without suppressing natural hormone rhythms.

hCG is a peptide hormone that mimics luteini.

HGH Frag 176-191 is a modified fragment of human growth hormone containing only the amino acid sequence responsible for its lipolytic (fat-burning) action, without the full range of GH effects. It selectively targets fat loss without affecting blood sugar or growth pathways.

Humanin is a mitochondrial-derived peptide (like MOTS-c) that activates AMPK, restoring energy production pathways; a specific humanin-to-PGC-1alpha link is not established in primary literature [PMID unverified — flagged 2026-06-19]. It represents a class of endogenous peptides encoded within mitochondrial DNA that regulate cellular survival and metabolism.

IGF-1 DES is a short-acting splice variant of IGF-1 with strong affinity for injured tissues.

IGF-1 LR3 is a long-acting analog of insulin-like growth factor 1 with direct action on muscle tissue. It increases contractile tissue, enhances recovery, and supports growth of high-frequency-use muscles.

Ipamorelin is most often combined with CJC-1295, a GHRH analog — the two act on different receptors and together produce a larger, more sustained GH release than either alone. It is also paired with GLP-1 drugs like semaglutide to help preserve lean mass during weight loss. These pairings are based on practitioner protocols, not controlled trials.

Ipamorelin is a selective growth-hormone secretagogue — a small five-amino- acid peptide that triggers the pituitary to release a natural pulse of growth hormone. It is valued for being selective: it raises GH with little effect on cortisol, prolactin, or appetite. It is studied for recovery, body composition, and sleep, and is not FDA-approved.

Kisspeptin is a hormone compound. Endogenous ligand for GPR54 (KISS1R).

KPV is a healing recovery compound. C-terminal tripeptide of alpha-MSH — potent anti-inflammatory via NF-kB pathway inhibition; enters nucleus to directly suppress inflammatory transcription; melanocortin receptor-independent action.

Liraglutide is a weight loss compound. GLP-1 receptor agonist with 97% homology to native GLP-1; C16 palmitoyl fatty acid side chain enables albumin binding, extending half-life.

Livagen is a synthetic tetrapeptide (Lys-Glu-Asp-Ala, "KEDA") from the Khavinson short-peptide bioregulator family. It is classed as a liver "Cytogen" and is studied for hepatic support and as an epigenetic regulator of chromatin and tissue-specific gene expression.

Livagen is the tetrapeptide Lys-Glu-Asp-Ala (KEDA), molecular weight ≈462 Da. It is structurally related to the other Khavinson Cytogens (Vilon, Vesugen, Epithalon).

LL-37 is a cathelicidin antimicrobial peptide involved in innate immunity that destroys bacteria, modulates inflammation, and supports tissue repair. Found naturally in neutrophils and epithelial tissues, it is used for gut healing, skin conditions, and immune rebalancing.

Melanotan I is a synthetic analog of alpha-MSH that stimulates melanin production for sunless tanning and potential photoprotection. Marketed pharmaceutically as afamelanotide, it is the more selective and safer cousin of Melanotan-II.

Melanotan II is a synthetic cyclic peptide analog of alpha-melanocyte- stimulating hormone, developed at the University of Arizona in the 1990s. It is a non-selective melanocortin receptor agonist used illicitly to stimulate skin tanning without UV exposure, and is colloquially called the "Barbie drug." It is not FDA-approved, and the FDA and other regulators have issued warnings against its use.

MK-677 (Ibutamoren) is an orally-active, non-peptide growth hormone secretagogue. It activates the ghrelin receptor (GHS-R1a) to amplify the body's own pulsatile growth hormone release, which in turn raises IGF-1. Its defining feature is that it works orally and is long-acting, unlike injectable GH-releasing peptides. It is not FDA-approved.

MOTS-c is a longevity compound. Mitochondrial-derived peptide — activates AMPK pathway, regulates folate-methionine cycle, improves metabolic homeostasis, enhances insulin sensitivity, modulates mTOR signaling.

NAD+ is a longevity compound. Essential coenzyme for 500+ enzymatic reactions — activates sirtuins (SIRT1-7), fuels PARP-mediated DNA repair, maintains mitochondrial electron transport chain, regulates NAD+/NADH redox balance.

Noopept is a synthetic nootropic peptide-derived compound that supports working memory and verbal fluency. It is considered one of the more potent racetam-like nootropics, though it is technically a dipeptide derivative rather than a racetam.

NSI-189 is a neurogenic compound that stimulates hippocampal neurogenesis and provides mood-lifting effects. It works on different aspects of neurogenesis and mood regulation than other cognitive peptides, making it especially effective in trauma-related depression.

Oxytocin is a neuropeptide hormone produced in the hypothalamus known as "the love hormone. " It plays a key role in emotional bonding, social connection, anxiety relief, and intimacy support.

P21 is a senolytic peptide that targets and reduces expression of p21, a key cell cycle inhibitor associated with cellular aging and senescence. Research shows it may restore regenerative potential in aged tissues and help regenerate neural pathways lost to age or stress.

PEG-MGF is a PEGylated splice variant of IGF-1 that activates satellite cells in muscle tissue. The PEGylation extends its half-life, enhancing systemic recovery effects post-exercise and making it effective for muscle atrophy reversal and tissue regeneration.

Pinealon is a synthetic neuroprotective tripeptide (Glu-Asp-Arg, "EDR") from the Khavinson Cytogen family. It is studied as a brain-targeted bioregulator that influences neuronal survival, serotonin synthesis and antioxidant defence through epigenetic regulation of gene expression.

Pinealon is the tripeptide Glu-Asp-Arg (EDR), molecular weight ≈418 Da. It is the neuro-targeted member of the Khavinson Cytogens, alongside Vilon (KE), Vesugen (KED) and Epithalon.

Pramlintide is an analog of the hormone amylin, co-secreted with insulin by pancreatic beta cells. It slows gastric emptying, suppresses post-meal glucagon, and promotes satiety, improving blood glucose control in type 1 and type 2 diabetes.

PT-141 is a sexual health compound. Melanocortin receptor agonist (MC3R/MC4R) — acts on hypothalamic neurons to modulate sexual desire and arousal via CNS pathways, not peripheral vasculature.

Retatrutide (development code LY3437943) is an investigational triple receptor agonist — it activates the GLP-1, GIP, and glucagon receptors at once. Being developed by Eli Lilly, it is the next step beyond dual GIP/ GLP-1 drugs like tirzepatide. The added glucagon-receptor activity is thought to increase energy expenditure. It is not FDA-approved and remains in clinical trials.

Retinalamin is a polypeptide bioregulator derived from bovine retinal tissue, used clinically in Russian ophthalmology for retinal protection and visual function support across conditions including diabetic retinopathy, glaucoma, and hereditary retinal degenerations.

Selank is a cognitive compound. Synthetic tuftsin analog with C-terminal Pro-Gly-Pro extension — modulates GABAergic system, stabilizes enkephalins, regulates IL-6 and monoamine metabolism, anxiolytic without sedation.

Semaglutide is a GLP-1 receptor agonist — a 31-amino-acid analog of the human incretin hormone GLP-1. It is FDA-approved as Ozempic and Rybelsus for type 2 diabetes and as Wegovy for chronic weight management. It works by reducing appetite, slowing gastric emptying, and improving blood-sugar control. A C-18 fatty-acid chain extends its half-life to allow once-weekly dosing.

Semax is a cognitive compound. Synthetic ACTH(4-7) analog with C-terminal Pro-Gly-Pro extension — enhances BDNF/NGF expression, modulates dopamine/serotonin systems, neuroprotective via anti-inflammatory and anti-apoptotic pathways.

Sermorelin is a growth hormone compound. Binds GHRH receptors on anterior pituitary somatotrophs, stimulating endogenous GH synthesis and pulsatile release via cAMP/PKA signaling.

SS-31 is a longevity compound. Targets cardiolipin in inner mitochondrial membrane — stabilizes electron transport chain, reduces oxidative stress, restores mitochondrial cristae structure and bioenergetics.

Svetinorm is a liver "Cytomax" — a natural polypeptide complex extracted from the liver tissue of young animals, in the Khavinson bioregulator family. It is marketed as a hepatoprotective bioregulator for liver-cell regeneration and is used in Russian clinical practice for fatty liver, alcohol/toxin damage, and hepatitis recovery. It is the natural organ-extract counterpart to the synthetic liver Cytogen Livagen.

TB-500 is a synthetic version of Thymosin Beta-4 (Tβ4), a naturally occurring 43-amino-acid peptide found in nearly all human and animal cells and the main actin-sequestering molecule in mammalian cells. It plays a central role in cell migration, wound healing, and tissue repair. Unlike BPC-157, which works best near the injury site, TB-500 is fully systemic. It is not FDA-approved.

Tesamorelin is a growth hormone compound. Modified GHRH(1-44) analog with N-terminal trans-3-hexenoic acid modification that increases stability and receptor affinity; stimulates pulsatile GH release from anterior pituitary via GHRHR/cAMP/PKA pathway.

Tesofensine (development code NS2330) is a small-molecule triple monoamine-reuptake inhibitor — it blocks reuptake of dopamine, noradrenaline and serotonin, raising synaptic levels of all three. It was originally developed for Parkinson's and Alzheimer's disease, failed in those indications, and was repurposed for obesity after trial participants lost weight. In a 203-patient Phase II obesity trial (TIPO-1, Astrup, Lancet 2008) the 0.5 mg dose produced roughly twice the weight loss of then-approved drugs. It is NOT a peptide despite living in peptide protocol libraries, and it is not FDA-approved.

"No DAC" (Mod GRF 1-29) is short-acting, with about a 30-minute half-life, producing discrete GH pulses that mimic natural physiology; it requires multiple daily doses. "With DAC" uses a Drug Affinity Complex that binds albumin, extending the half-life to roughly 8 days for sustained GH elevation and once- or twice-weekly dosing. Many practitioners prefer no DAC to preserve pulsatility.

PT-141 (bremelanotide) is the FDA-approved derivative developed from Melanotan II, selectively targeting melanocortin receptors for sexual function (hypoactive sexual desire disorder). Melanotan II is non-selective across all five melanocortin receptors, which adds tanning, appetite, and broader off-target effects plus the associated safety burden. PT-141 is the regulated option when sexual function is the goal.

Both are healing peptides often stacked together, but they act differently. TB-500 is fully systemic — injected anywhere, it travels to injury sites body-wide for tissue remodeling, angiogenesis, and cell migration. BPC-157 works best injected locally near the injury for targeted repair. Combining them is the most popular injury-recovery stack because they cover both systemic and local healing pathways.

Thymalin is a thymus bioregulator peptide complex that restores thymus function, supports immune cell education, and modulates immune overactivation.

Thymosin Alpha-1 is a immune compound. Immune modulator — enhances T-cell maturation, dendritic cell function, NK cell activity, and TLR signaling; modulates Treg/Teff balance.

Tirzepatide is a dual GIP/GLP-1 receptor agonist — a single 39-amino-acid peptide that activates two incretin receptors at once. It is FDA-approved as Mounjaro for type 2 diabetes and as Zepbound for weight management. By engaging both the GIP and GLP-1 pathways it produces larger metabolic effects than GLP-1-only drugs. It is dosed once weekly.

Triptorelin is a GnRH agonist that reduces sex hormone levels through receptor desensiti.

Ventfort is a vascular "Cytomax" in the Khavinson bioregulator family — a natural polypeptide complex extracted from the blood-vessel wall and endothelial tissue of young animals, rather than a single synthetic peptide. It is marketed to support endothelial repair, microcirculation and vessel elasticity and to counter age-related vascular stiffness. It is the organ-extract counterpart to the synthetic vascular peptide Vesugen (KED).

Ventfort does not have a single defined amino-acid sequence. As a Cytomax it is a natural mixture of peptides purified from vascular tissue, not one molecule. This is the key difference from its synthetic Cytogen counterpart Vesugen, which is the defined tripeptide Lys-Glu-Asp (KED, ~390 Da). No peer-reviewed sequence or molecular-weight characterization of Ventfort exists.

Vesugen is a synthetic tripeptide (Lys-Glu-Asp, "KED") from the Khavinson short-peptide bioregulator family. It is the vascular "Cytogen," studied as an epigenetic regulator of endothelial cells for vascular repair and anti-atherosclerotic effects.

Vesugen is the tripeptide Lys-Glu-Asp (KED), molecular weight ≈390 Da. It is one of the Khavinson Cytogens, related to Vilon (KE), Livagen (KEDA) and Epithalon.

Vilon is a synthetic dipeptide (Lys-Glu, also written "KE") from the Khavinson family of short-peptide bioregulators developed at the St. Petersburg Institute of Bioregulation and Gerontology. It is classed as a thymic/immune "Cytogen" and is studied as a geroprotector that modulates immune-related gene expression.

Vilon is the dipeptide L-lysyl-L-glutamic acid (Lys-Glu / KE), molecular weight ≈275 Da. It is one of the shortest peptides reported to have biological activity.

VIP is a immune gut compound. Binds VPAC1 and VPAC2 receptors (Class B GPCRs); activates cAMP/PKA signaling.