Peptide Library

Compound-by-compound overviews. Mechanism, evidence level, reported research uses, and safety considerations.

Where to start

Editorial routes into the library. Not personalization — just useful starting points.

Categories
Fat Loss & Metabolism
Compounds studied for body-composition, glycaemic control, and metabolic health.
Categories
Repair & Regeneration
Compounds studied for wound healing, tissue repair, and musculoskeletal recovery.
Categories
Cellular Health
Compounds studied for mitochondrial function, redox balance, and cellular integrity.
Categories
Muscle & Performance
Compounds studied for GH-axis pulsatility, lean-mass support, and performance-adjacent research.

Showing all 33 peptides

PT-141
Hormonal & Reproductive ResearchModerate Human Evidence
A cyclic heptapeptide melanocortin receptor agonist. It acts predominantly at the melanocortin-4 receptor (MC4R) in the central nervous system, with weaker activity at MC1R, MC3R and MC5R. The MC4R-expressing hypothalamic neurones it engages are part of the central sexual-response circuitry — the same neural nodes implicated in appetitive sexual desire. The molecule is bremelanotide, marketed as Vyleesi by AMAG Pharmaceuticals (originally licensed from Palatin Technologies), and FDA-approved on 2019-06-21 for hypoactive sexual desire disorder (HSDD) in premenopausal women as a 1.75 mg subcutaneous injection given on demand roughly 45 minutes before anticipated sexual activity.
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Melanotan I
Skin & Pigmentation ResearchModerate Human Evidence
A 13-amino-acid linear α-MSH analogue with two stabilising substitutions (norleucine at position 4 and D-phenylalanine at position 7) that greatly extend its half-life relative to native α-MSH. It is a potent melanocortin receptor agonist, and its clinical effect is mediated principally through the MC1R on melanocytes: MC1R activation drives conversion of the light red/yellow pigment pheomelanin to the darker, more photoprotective eumelanin, producing a controlled skin darkening that in erythropoietic protoporphyria (EPP) increases tolerance to sunlight. As afamelanotide (Scenesse), the compound is delivered as a 16 mg controlled-release biodegradable subcutaneous implant. It is authorised by the EMA (2014) and FDA-approved on 2019-10-08 for the reduction of phototoxicity in adult EPP patients.
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Melanotan II
Skin & Pigmentation ResearchPreclinical Evidence
A synthetic cyclic heptapeptide α-MSH analogue with broad activity across all four peripheral melanocortin receptor subtypes: MC1R (skin darkening via eumelanin), MC3R and MC4R (central sexual-response circuitry and appetite regulation) and MC5R (sebaceous / exocrine gland activity). It has never been approved by any regulator. It circulates as a grey-market cosmetic tanning and sexual-response peptide via research-supply channels, and multiple national regulators — including the UK MHRA, Norwegian Medicines Agency, Irish HPRA, and Australian TGA — have issued specific warnings against its cosmetic use. Its historical significance is as the research tool whose accidental sexual-response observation launched the Palatin bremelanotide programme.
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SS-31
Cellular HealthModerate Human Evidence
A synthetic aromatic-cationic tetrapeptide originally developed by Hazel Szeto and Peter Schiller at Cornell University. Unlike most peptides, elamipretide concentrates in the inner mitochondrial membrane at 1,000-fold higher levels than in cytoplasm, where it binds cardiolipin — the phospholipid that stabilises cristae architecture and holds the electron-transport-chain complexes together. Cardiolipin binding stabilises cristae structure, preserves supercomplex assembly, restores efficient ATP synthesis and reduces reactive-oxygen-species leakage. Licensed to Stealth BioTherapeutics, elamipretide has been developed through a phase-3 randomised placebo-controlled trial (TAZPOWER) in Barth syndrome — a rare X-linked disorder of the cardiolipin remodelling enzyme tafazzin — and subsequently received FDA approval as Forzinity for that indication.
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Thymosin Alpha-1
Immunology & InflammationModerate Human Evidence
A 28-amino-acid N-acetylated peptide originally isolated by Allan Goldstein and colleagues from bovine thymus in 1972 as part of 'fraction 5'. It is a naturally occurring proteolytic product of prothymosin alpha in humans. Thymosin alpha-1 modulates both innate and adaptive immunity, principally by signalling through Toll-like receptors 2 and 9 on dendritic cells, enhancing dendritic cell maturation, promoting Th1-polarised T-cell responses, and increasing natural killer cell activity. It is approved as thymalfasin (Zadaxin, SciClone Pharmaceuticals) in more than 35 countries — including China, Argentina, Brazil, Italy, Mexico, Philippines and Singapore — for chronic hepatitis B, adjunctive treatment of chronic hepatitis C, and various immune-restoration indications. It has never been FDA-approved in the United States or EMA-authorised in the European Union.
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Kisspeptin
Hormonal & Reproductive ResearchEarly Human Evidence
Kisspeptins are endogenous peptides produced by the KISS1 gene and cleaved into several bioactive forms (kisspeptin-54, -14, -13, -10). All share the C-terminal decapeptide (kisspeptin-10) that binds KISS1R (GPR54), a G-protein-coupled receptor expressed on GnRH neurones of the hypothalamic arcuate nucleus. Activation of KISS1R triggers pulsatile GnRH release, which in turn drives LH and FSH secretion from the pituitary. Kisspeptin is now understood to be the primary upstream regulator of the entire hypothalamic-pituitary-gonadal axis; loss-of-function mutations in KISS1R cause hypogonadotropic hypogonadism, and the peptide has been studied in humans by the Dhillo group and others as a physiological substitute for GnRH in hypothalamic amenorrhoea and in assisted-reproduction protocols. There is no approved kisspeptin therapeutic; the compound remains in the investigational phase.
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Selank
Cognition & MoodEarly Human Evidence
A synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed at the Institute of Molecular Genetics of the Russian Academy of Sciences (Myasoedov group) and the Zakusov Institute of Pharmacology. Its parent sequence tuftsin (Thr-Lys-Pro-Arg) is a naturally occurring tetrapeptide released from the IgG heavy chain that modulates macrophage and neutrophil activity; the added -Pro-Gly-Pro C-terminal tripeptide dramatically increases the peptide's plasma stability and centrally-active anxiolytic profile. Selank has been registered in Russia and some CIS countries as a prescription anxiolytic under the brand name Selank® (Селанк) as a 0.15% intranasal solution. Mechanism studies indicate BDNF and NGF upregulation, modulation of monoamine and GABAergic systems, and inhibition of enkephalin-degrading enzymes (protecting endogenous opioid tone). It has no MHRA / EMA / FDA authorisation.
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Semax
Cognition & MoodEarly Human Evidence
A synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) that reproduces the ACTH(4-10) neuropeptide fragment — the portion of adrenocorticotropic hormone stripped of its corticotropic activity — extended at the C-terminus with a Pro-Gly-Pro tail that dramatically increases plasma stability and central nervous system penetration. Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences (Ivanov, Myasoedov and colleagues), Semax has been registered in Russia since 1994. Its approved indications include acute ischaemic stroke (Semax 1% intranasal), transient ischaemic attack, discirculatory encephalopathy, chronic fatigue, optic nerve atrophy and cognitive impairment. Mechanism studies indicate BDNF and NGF upregulation, monoamine and cholinergic modulation, and neuroprotection through reduced excitotoxicity. It has no MHRA / EMA / FDA authorisation.
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DSIP
Cognition & MoodPreclinical Evidence
A nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) isolated in 1977 by Marcel Monnier and Guido Schoenenberger at the University of Basel from the cerebral venous blood of rabbits subjected to electrical thalamic stimulation that induced slow-wave (delta) sleep. The peptide was named for the electroencephalographic signature it was thought to induce. Fifty years of subsequent research has broadened the picture without fully resolving it: DSIP has been shown to modulate GABAergic, serotonergic and monoaminergic tone, to influence adrenocorticotropic hormone secretion patterns, and to interact with opioid systems. It crosses the blood-brain barrier. It is not a classical receptor agonist — no single receptor accounts for its whole pharmacology. Small human clinical studies conducted mostly in the 1980s and 1990s in narcolepsy, chronic pain and opioid withdrawal produced mixed signals. It has never been approved by any regulator.
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NAD+
Cellular HealthEarly Human Evidence
NAD+ (nicotinamide adenine dinucleotide, oxidised form) is a pyridine-nucleotide coenzyme — chemically a dinucleotide, not a peptide. It sits at the centre of cellular redox biology: NAD+ / NADH cycling drives ATP production through the electron transport chain, and NAD+ is the required substrate for the sirtuin family of deacetylases (SIRT1–7) that regulate gene expression, mitochondrial biogenesis (via PGC-1α), inflammation and DNA-damage responses. NAD+ is also consumed by PARP-1 during DNA-strand-break repair and by CD38 during immune-cell signalling. Endogenous NAD+ levels decline with age, and this decline is thought to contribute to reduced sirtuin activity, mitochondrial dysfunction and impaired DNA repair. Injectable NAD+ has no FDA-approved therapeutic indication; its metabolic precursors (nicotinamide riboside — NR, nicotinamide mononucleotide — NMN) are widely sold as oral supplements. The compound is included in this catalog because the Healthy Mango PDF covers it alongside peptides, not because it is one.
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Glutathione (GSH)
Cellular HealthEarly Human Evidence
Glutathione is a tripeptide of glutamate, cysteine and glycine, distinguished from most other peptides by a non-standard γ-carboxyl bond linking glutamate to cysteine that protects the molecule from routine peptidase degradation. It is present at millimolar concentrations in essentially every human cell, where it is the primary intracellular thiol antioxidant. Its cysteine thiol (-SH) group reduces reactive oxygen species directly; it conjugates with toxins and xenobiotics via glutathione S-transferase for hepatic Phase II export; it recycles oxidised vitamin C and vitamin E back to their active forms; it supports T-cell proliferation and NK-cell cytotoxicity; and it inhibits tyrosinase, the enzyme that catalyses the rate-limiting step of melanin synthesis — the mechanistic basis for glutathione's cosmetic skin-lightening effect at sustained doses. Oral glutathione has weak bioavailability; liposomal and sublingual formulations claim to improve absorption. Injectable IV or subcutaneous glutathione is used off-label for cosmetic skin lightening in several jurisdictions, a use that regulators including the Philippines FDA have specifically warned against for safety reasons.
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Aura
Repair & RegenerationResearch BlendPreclinical Evidence
A three-component research blend combining GHK-Cu 50 mg, BPC-157 10 mg and KPV 10 mg in a single lyophilized vial (70 mg total). The three components address distinct but complementary layers of tissue repair: GHK-Cu modulates the expression of thousands of genes involved in ECM remodelling, collagen and elastin synthesis, angiogenesis and scarless healing; BPC-157 supports VEGF-driven angiogenesis, fibroblast migration and collagen production at the repair site; and KPV suppresses the NF-κB inflammatory pathway that would otherwise antagonise the ECM and vascular repair activities of the other two components. At the reference reconstitution (5 mL bacteriostatic water → 10 mg/mL GHK-Cu + 2 mg/mL BPC-157 + 2 mg/mL KPV) and 0.2 mL injection volume, all three components fall within their individually-established therapeutic ranges — a distinguishing feature of Aura relative to other multi-component repair blends. No blend-specific FDA authorisation exists; the individual components have their own regulatory profiles (see the component compound pages).
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Glow
Repair & RegenerationResearch BlendPreclinical Evidence
A three-component research blend combining GHK-Cu 50 mg, BPC-157 10 mg and TB-500 10 mg in a single lyophilized vial (70 mg total). Structural repair with skin rejuvenation: GHK-Cu at the gene-expression / ECM signalling layer, BPC-157 at the vascular / fibroblast layer, and TB-500 at the cellular migration and cytoskeletal-remodelling layer. The mechanism story is complementary rather than redundant — each component addresses a distinct rate-limiting step in tissue repair. Relative to Aura, Glow substitutes TB-500 for KPV, trading inflammatory-environment control for cellular-migration capacity. The trade-off worth being honest about: at the 0.2 mL reference injection, TB-500 is delivered at maintenance levels rather than acute-injury loading levels. No FDA blend authorisation exists; the individual components have their own regulatory profiles.
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Klow
Repair & RegenerationResearch BlendPreclinical Evidence
A four-component research blend that combines all three peptide families addressed by the other repair blends plus the anti-inflammatory KPV component. Composition: GHK-Cu 50 mg + TB-500 10 mg + BPC-157 10 mg + KPV 10 mg = 80 mg total. The mechanism story covers all four rate-limiting layers of tissue repair: GHK-Cu at the gene-level ECM signalling layer, TB-500 at the cellular migration and cytoskeletal remodelling layer, BPC-157 at the vascular supply and fibroblast layer, and KPV at the inflammatory-environment control layer. In effect, Klow is Glow plus KPV — adding NF-κB pathway suppression to the three mechanistic components of Glow — and Aura plus TB-500 — adding cellular migration to the three components of Aura. It is the most comprehensive of the repair blends when all four components are available and the intended use warrants their combined effect.
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Selank / Semax Blend
Cognition & MoodResearch BlendEarly Human Evidence
A two-component neuro / nootropic research blend combining Selank 5 mg + Semax 5 mg (10 mg total) in a single lyophilized vial. Both compounds come from the same Russian regulator-peptide tradition at the Institute of Molecular Genetics — see the individual Selank and Semax pages. The blend pairs their complementary neurological effects: Selank as a positive allosteric modulator at a benzodiazepine-independent GABA-A site (anxiolysis without sedation or dependence) and Semax as an ACTH(4-10)-derived BDNF and NGF upregulator (cognitive activation and neuroplasticity). The two act on non-overlapping receptor systems and produce no pharmacological conflict. Both routes documented in the source PDF are available: subcutaneous injection and intranasal (bacteriostatic water for subQ, sterile saline for intranasal).
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BPC-157 / TB-500 Blend
Repair & RegenerationResearch BlendPreclinical Evidence
A two-component tissue-repair research blend combining BPC-157 and TB-500 in a 1:1 ratio, supplied as either a 5/5 mg (10 mg total) or 10/10 mg (20 mg total) lyophilized vial. The mechanistic rationale is direct: BPC-157 addresses the vascular supply and fibroblast recruitment side of tissue repair through VEGF-driven angiogenesis and NO-mediated signalling; TB-500 addresses the cellular migration side through actin polymerisation dynamics that enable repair cells and stem cells to reach injury sites. Together the two address the two most commonly rate-limiting layers of tissue repair — vascular supply and cellular movement — in a single reconstitution. Simpler than running the two peptides in parallel from separate vials.
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CJC-1295 / Ipamorelin Blend
Muscle & PerformanceResearch BlendEarly Human Evidence
The gold-standard GH secretagogue stack in a single vial: CJC-1295 No DAC 5 mg + Ipamorelin 5 mg = 10 mg total. The two peptides drive growth-hormone release through two distinct receptor systems that are synergistic when combined. CJC-1295 No DAC activates GHRH receptors on pituitary somatotrophs, producing a short, sharp GH pulse. Ipamorelin simultaneously activates ghrelin (GHSR) receptors, amplifying the same GH pulse through a separate pathway. The two signals are synergistic — the combined GH release is significantly greater than the additive sum, because pulsatile activation of both receptor systems produces a physiologic GH pulse larger than either component alone can generate. Ipamorelin does not elevate cortisol, prolactin or ACTH — an important selectivity property that makes this blend cleaner than older ghrelin-mimetic combinations. Both components are optimally dosed at 0.1–0.15 mL per injection, both are well-characterised individually, and both are within their individually-established therapeutic ranges in the blend format.
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Tesamorelin / Ipamorelin Blend
Fat Loss & MetabolismResearch BlendEarly Human Evidence
A two-component GH-axis research blend: Tesamorelin 5 mg + Ipamorelin 5 mg = 10 mg total. The pairing combines Tesamorelin (a stabilised GHRH analogue documented for visceral-fat reduction in the peer-reviewed GHRH-analogue literature) with Ipamorelin (a selective ghrelin-receptor agonist that adds GH pulse amplification without cortisol / prolactin / ACTH elevation). The mechanistic argument is similar to the CJC-1295 / Ipamorelin blend — dual-pathway GH stimulation — but with a Tesamorelin backbone chosen specifically for its documented visceral-fat-reduction pharmacology. The 1:1 vial ratio produces an inherent dose trade-off worth naming honestly: the 2 mg Tesamorelin research reference (0.4 mL of the reconstituted blend) delivers 1 mg of Ipamorelin — meaningfully above its optimal 0.25–0.375 mg range. The 0.2 mL compromise dose gives 0.5 mg of each — Tesamorelin below its research reference and Ipamorelin above its optimal.
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Semaglutide
Fat Loss & MetabolismStrong Human Evidence
A once-weekly (subcutaneous) or once-daily (oral) GLP-1 receptor agonist approved by the FDA and EMA under distinct brand names for type 2 diabetes (Ozempic, Rybelsus), chronic weight management (Wegovy), and cardiovascular risk reduction in specified populations. It signals through a single incretin receptor, without direct GIP or glucagon receptor activity.
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Tesamorelin
Fat Loss & MetabolismModerate Human Evidence
A synthetic full-length analogue of growth hormone-releasing hormone (GHRH) that binds the pituitary GHRH receptor and stimulates the body's own pulsatile release of growth hormone. Research contexts include visceral fat reduction, body composition, and hepatic fat — a research-use peptide that preserves the physiologic GH pulse rather than replacing GH directly.
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Sermorelin
Muscle & PerformanceModerate Human Evidence
The shortest peptide analogue of endogenous growth hormone-releasing hormone (GHRH), consisting of amino acids 1–29 with a C-terminal amide. Binds the pituitary GHRH receptor and stimulates a short, sharp physiologic GH pulse. Historically approved by the FDA as Geref for pediatric GH deficiency in 1990; the NDA was withdrawn in 2008 for commercial reasons. Modern use is exclusively via compounding pharmacies; there is no currently marketed FDA-approved product.
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CJC-1295 (No DAC)
Muscle & PerformanceModerate Human Evidence
A chemically modified analogue of GHRH(1-29) — the biologically active fragment of endogenous growth hormone-releasing hormone — engineered with four amino acid substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) that resist enzymatic degradation without extending the half-life through albumin binding. Produces a short, sharp physiologic GH pulse. Research-only; no FDA or EMA approval. Distinct from CJC-1295 DAC, which adds an albumin-binding linker and has an ~8-day half-life.
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CJC-1295 DAC
Muscle & PerformanceModerate Human Evidence
The identical GHRH(1-29) backbone as CJC-1295 No DAC — same four amino acid substitutions, same receptor — with one additional chemical group: a maleimidopropionic acid (MPA) linker that covalently binds free serum albumin after injection. The albumin conjugation extends the plasma half-life from ~30 minutes to approximately 8 days. But it also transforms the pharmacologic signal: instead of a pulsatile GH release, the drug produces a sustained flat elevation. Not a stronger pulse — a fundamentally different drug.
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Ipamorelin
Muscle & PerformanceModerate Human Evidence
A synthetic pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2) that binds the ghrelin receptor GHSR-1a on pituitary somatotrophs and hypothalamic neurons, triggering GH release through a pathway parallel and additive to GHRH. Distinguished from older GH-releasing peptides (GHRP-2, GHRP-6) by selectivity: at doses producing GH release, ipamorelin does not activate the ACTH/cortisol or prolactin axes. Research-only; no FDA or EMA approval.
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BPC-157
Repair & RegenerationEarly Human Evidence
A synthetic 15-amino-acid fragment corresponding to a portion of a protein found in human gastric juice. Preclinical work — almost all of it from Sikiric's laboratory at the University of Zagreb — describes broad tissue-protective effects across gut, tendon, muscle, bone, brain, and vascular endpoints, with proposed mechanisms centred on VEGF-mediated angiogenesis, fibroblast migration, and modulation of the nitric oxide system. The compound has no approved indication in any jurisdiction and no completed phase-2 or phase-3 randomised trial in humans.
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TB-500
Repair & RegenerationEarly Human Evidence
A 17-amino-acid synthetic peptide corresponding to the N-terminal actin-binding region of thymosin β4 — a 43-amino-acid endogenous protein. TB-500 is NOT thymosin β4 itself. Popular sources routinely treat the two as interchangeable; they are not. The mechanistic hypothesis is that the actin-sequestering region of Tβ4 alone recapitulates a subset of the parent protein's cell-migration and wound-healing effects. Human evidence for TB-500 specifically is essentially absent. The compound originated in equine veterinary use and is on the WADA prohibited list.
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KPV
Immunology & InflammationEarly Human Evidence
A three-amino-acid peptide (Lys-Pro-Val) that constitutes the C-terminal fragment of α-melanocyte-stimulating hormone. KPV retains α-MSH's anti-inflammatory activity while losing its pigmentation, appetite, and sexual-arousal activities — the pharmacological signature of the melanocortin receptors that the parent hormone binds. The scientifically interesting fact is that KPV's anti-inflammatory effect appears to be MC-receptor-independent: it enters cells via the PepT1 oligopeptide transporter and modulates NF-κB signalling intracellularly. Research-only; no approved indication in any jurisdiction.
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GHK-Cu
Repair & RegenerationModerate Human Evidence
An endogenous copper-binding tripeptide (glycyl-L-histidyl-L-lysine complexed with copper(II)) first isolated from human plasma in 1973. GHK-Cu has the broadest gene-expression footprint characterised for any small research peptide — genome-wide microarray studies catalogue approximately 4200 human genes significantly modulated at physiological concentrations. Mechanistically, GHK-Cu functions as a copper-delivery vehicle: the tripeptide chelates and delivers copper into cells, where copper acts as an essential cofactor for enzymes involved in extracellular matrix synthesis, angiogenesis, antioxidant defense, and DNA repair. Approved and marketed for topical cosmetic use in many jurisdictions; not FDA-approved for systemic therapeutic indications.
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Epitalon
Longevity & Healthy AgingPreclinical Evidence
A synthetic four-amino-acid peptide (Ala-Glu-Asp-Gly) distilled as the proposed active fragment of Epithalamin, a pineal-gland extract characterised in the 1970s at the St. Petersburg Institute of Bioregulation and Gerontology. In the Khavinson-school framework it is a 'peptide bioregulator' — a short sequence proposed to modulate gene expression in pineal and other endocrine tissues. Reported effects in Russian-lab work include melatonin-rhythm normalisation, restoration of aged-animal circadian patterns, and elevation of telomerase activity in cultured somatic cells. Independent external replication of the most-cited claims — especially the telomerase and lifespan-extension findings — is limited, and no Western regulatory agency has authorised Epitalon for any indication.
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AOD-9604
Fat Loss & MetabolismEarly Human Evidence
A modified 15-amino-acid fragment corresponding to the C-terminus of human growth hormone (residues 177–191) with an added N-terminal tyrosine, designed at Monash University in the 1990s to isolate the lipolytic activity of hGH from its growth-signalling activity. Preclinical work described increased lipolysis and inhibition of lipogenesis in adipose tissue models without the anabolic signalling of full-length hGH. The compound was taken into human phase 2b obesity trials by Metabolic Pharmaceuticals; the 2007 12-week randomised placebo-controlled trial did not meet its primary weight-loss endpoint. The compound was subsequently repositioned as a 'generally recognised as safe' (GRAS) ingredient for functional-food applications — a regulatory pathway distinct from FDA drug approval, which the compound has never received.
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MOTS-c
Cellular HealthPreclinical Evidence
A 16-amino-acid peptide encoded within a short open reading frame in the mitochondrial 12S ribosomal RNA gene — one of a small class of 'mitochondrial-derived peptides' whose defining feature is that they originate from the mitochondrial genome rather than the nuclear genome. First characterised by Lee, Cohen and colleagues at USC in 2015. Proposed to function as a mitochondrion-to-nucleus retrograde signal, with reported downstream activation of AMP-activated protein kinase (AMPK) and modulation of glucose metabolism and insulin sensitivity. Preclinical work in mice describes exercise-mimetic effects on skeletal muscle glucose handling and running capacity. Human data are dominated by circulating-level correlational studies (levels lower in aged, obese, and diabetic populations); no completed phase-2 or phase-3 interventional trial of exogenous MOTS-c in humans has been published.
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Retatrutide
Fat Loss & MetabolismModerate Human Evidence
An investigational once-weekly molecule that activates three receptors at once — GIP, GLP-1, and glucagon. In Phase 3 clinical development (Eli Lilly's TRIUMPH program) for obesity and type 2 diabetes. Not approved by any regulator; no approved commercial formulation; no standardized public reconstitution instructions.
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Tirzepatide
Fat Loss & MetabolismStrong Human Evidence
A single molecule that activates GIP and GLP-1 receptors across the pancreas, gut, and brain. Tirzepatide is approved by the FDA and EMA for specified indications involving type 2 diabetes and chronic weight management, under distinct brands and regulatory labeling.
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Recently added

The newest 33 entries in the library.

Tesamorelin / Ipamorelin Blend
Added July 13, 2026
CJC-1295 / Ipamorelin Blend
Added July 13, 2026
BPC-157 / TB-500 Blend
Added July 13, 2026
Selank / Semax Blend
Added July 13, 2026
Klow
Added July 13, 2026
Glow
Added July 13, 2026

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Semaglutide vs Tirzepatide
Two of the most extensively studied incretin-based therapies — approved and marketed in the same therapeutic areas, but with different receptor profiles, different phase-3 programs, and different published outcomes. This page compares what the peer-reviewed literature and regulatory documentation currently support for each.
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Compare
Tirzepatide vs Retatrutide
Two incretin-based peptides in the same broad family, but at very different stages of development. This page compares what the peer-reviewed literature currently supports on each — regulatory status, receptor targets, evidence tier, and headline efficacy from published phase-3 trials.
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Compare
BPC-157 vs TB-500
These two peptides are the most-discussed pair in the tissue-repair conversation, and they are also the most-conflated. In practice they share none of what usually justifies grouping compounds: their origins are unrelated, their mechanisms are unrelated, and the shape of the evidence supporting each is structurally different. This page walks through those distinctions.
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Compare
KPV vs GHK-Cu
Two small, endogenously-derived peptides that get grouped in discussions about anti-inflammatory and skin peptides. They share molecular scale — both are tripeptides — and their mechanisms are both proposed to be intracellular rather than classical receptor-mediated. Everything else about their evidence structures, use cases, and regulatory status differs, in ways that are worth reading precisely.
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Tesamorelin vs Sermorelin
Two GHRH analogues built for the same fundamental job — stimulating the pituitary's own pulsatile release of growth hormone — but at very different points in structure, half-life, and regulatory history. This page compares what the peer-reviewed literature and regulatory documentation currently support for each.
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CJC-1295 (No DAC) vs Sermorelin
Two GHRH(1-29)-based signals. Sermorelin is the native sequence; CJC-1295 No DAC is the same sequence with four amino acid substitutions that resist enzymatic degradation. This page compares what the peer-reviewed literature currently supports on each.
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CJC-1295 No DAC vs CJC-1295 DAC
The two forms share an identical GHRH(1-29) backbone with the same four amino acid substitutions. The Drug Affinity Complex (DAC) — a single maleimidopropionic acid linker that covalently binds serum albumin — is the only chemical difference. Every downstream pharmacologic property flows from that one addition. This page reads out those differences precisely.
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AOD-9604 vs Semaglutide
Two compounds pursued as pharmacological approaches to weight loss, from opposite starting points and with opposite clinical results. AOD-9604 was designed as a lipolytic fragment of human growth hormone; its 2007 phase 2b did not meet its primary endpoint and its pharmaceutical program was discontinued. Semaglutide came from the incretin research tradition, obtained FDA approval for chronic weight management in 2021, and produced a large clinical evidence base. This page presents the two side by side to make each visible in the other's context.
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Peptide Library

Where to start

PT-141

Melanotan I

Melanotan II

SS-31

Thymosin Alpha-1

Kisspeptin

Selank

Semax

DSIP

NAD+

Glutathione (GSH)

Aura

Glow

Klow

Selank / Semax Blend

BPC-157 / TB-500 Blend

CJC-1295 / Ipamorelin Blend

Tesamorelin / Ipamorelin Blend

Semaglutide

Tesamorelin

Sermorelin

CJC-1295 (No DAC)

CJC-1295 DAC

Ipamorelin

BPC-157

TB-500

KPV

GHK-Cu

Epitalon

AOD-9604

MOTS-c

Retatrutide

Tirzepatide

Recently added

Recently updated

Stay ahead of the research.

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PT-141

Melanotan I

Melanotan II

SS-31

Thymosin Alpha-1

Kisspeptin

Selank

Semax

DSIP

NAD+

Glutathione (GSH)

Aura

Glow

Klow

Selank / Semax Blend

BPC-157 / TB-500 Blend

CJC-1295 / Ipamorelin Blend

Tesamorelin / Ipamorelin Blend

Semaglutide

Tesamorelin

Sermorelin

CJC-1295 (No DAC)

CJC-1295 DAC

Ipamorelin

BPC-157

TB-500

KPV

GHK-Cu

Epitalon

AOD-9604

MOTS-c

Retatrutide

Tirzepatide