Peptide Library

Endogenous tripeptide (glutamate-cysteine-glycine) and the body's master antioxidant. Neutralizes reactive oxygen species, regenerates vitamins C and E, detoxifies xenobiotics via conjugation, and inhibits melanin synthesis by switching from eumelanin to pheomelanin production.

Lipotropic injection containing methionine, inositol, choline, and commonly supplemented with L-carnitine, B12, and B-complex vitamins. Enhances hepatic fat metabolism, supports methylation pathways, and promotes bile flow for improved lipid processing.

Lipopeptide consisting of a palmitoyl group linked to the pentapeptide KTTKS (a collagen I fragment). Acts as a matrikine, signaling fibroblasts to increase collagen I, III, and IV synthesis, fibronectin production, and hyaluronic acid production via TGF-beta pathway activation.

Synthetic analog of alpha-melanocyte stimulating hormone (alpha-MSH). Binds melanocortin-1 receptor (MC1R) on melanocytes, stimulating eumelanin production and distribution. Produces gradual, UV-independent tanning. Does not significantly affect sexual function (unlike MT-II).

Non-selective melanocortin receptor agonist. Activates MC1R (tanning), MC3R/MC4R (sexual arousal and appetite suppression), and MC5R (exocrine gland function). Produces tanning, increases sexual arousal, and suppresses appetite through simultaneous multi-receptor activation.

Octapeptide that mimics the N-terminal of SNAP-25, a key protein in the SNARE complex responsible for neurotransmitter release at neuromuscular junctions. Competitively inhibits SNARE complex formation, reducing muscle contraction intensity and thereby reducing expression lines.

Porcine brain-derived peptide preparation containing low-molecular-weight neuropeptides and free amino acids. Exhibits neurotrophic activity mimicking BDNF, GDNF, NGF, and CNTF. Promotes neuronal sprouting, synaptogenesis, and neurogenesis. Reduces neuroinflammation.

Angiotensin IV analog that activates hepatocyte growth factor (HGF) signaling via the c-Met receptor. Promotes synaptogenesis, dendritic spine formation, and neuronal connectivity. Approximately 10 million times more potent than BDNF at promoting synaptic connections.

Nonapeptide that modulates sleep architecture by increasing delta wave activity during slow-wave sleep. Acts through multiple mechanisms including GABA modulation, serotonergic signaling, and suppression of corticotropin-releasing hormone. Does not induce sedation but improves sleep quality.

Synthetic heptapeptide analog of endogenous tuftsin with a Pro-Gly-Pro stabilizing sequence. Modulates IL-6, BDNF, and enkephalin expression. Anxiolytic effects mediated through GABAergic modulation without sedation or dependence. Enhances memory consolidation.

Synthetic analog of ACTH 4-10 fragment with a Pro-Gly-Pro C-terminal extension. Increases BDNF and NGF expression in the hippocampus. Enhances attention, memory, and learning without hormonal effects of full-length ACTH. Neuroprotective against oxidative stress.

Endogenous 28-amino-acid neuropeptide with broad physiological roles. Potent vasodilator, bronchodilator, and immunomodulator. Promotes neuronal survival, regulates circadian rhythm via SCN, inhibits NF-kB-mediated inflammation, and modulates gut-brain axis signaling.

Adamantane-modified peptide designed for enhanced blood-brain barrier penetration and metabolic stability. The adamantane cage structure protects the peptide from enzymatic degradation while improving lipophilicity and cellular uptake for CNS-mediated metabolic effects.

Peptidomimetic that targets prohibitin on adipose vasculature. Binds to ANXA2 receptors on blood vessels supplying white adipose tissue, triggering targeted apoptosis of fat tissue endothelial cells. Causes selective fat tissue vascular disruption and subsequent fat cell death.

Naturally occurring heptapeptide isolated from the skin of South American tree frogs (Phyllomedusa). Potent and selective mu-opioid receptor agonist — approximately 30-40 times more potent than morphine. Contains D-alanine, which is rare in natural peptides.

D-retro-inverso peptide that disrupts the interaction between FOXO4 and p53 in senescent cells. Forces p53 into the mitochondria of senescent cells, triggering selective apoptosis (senolysis). Clears senescent cells without affecting healthy cells.

Fragment of proenkephalin that modulates opioid receptor signaling in adipose tissue. Promotes brown adipose tissue thermogenesis and white adipose tissue browning. Enhances uncoupling protein 1 (UCP1) expression, increasing non-shivering thermogenesis and energy expenditure.

Chimeric peptide combining an HDM-2 binding domain with a cell-penetrating sequence. Selectively targets cells with membrane-associated HDM-2 (overexpressed in many cancer cells), creating pores that trigger necrosis. Spares normal cells lacking surface HDM-2.

Soluble activin receptor type IIB fusion protein that acts as a decoy receptor, binding and neutralizing myostatin, activin, GDF-11, and other TGF-beta superfamily ligands. Removes multiple negative regulators of muscle growth simultaneously.

Activin-binding protein that potently inhibits myostatin, a negative regulator of muscle growth. Blocking myostatin removes the genetic brake on muscle hypertrophy. Also inhibits FSH (follicle-stimulating hormone) as activin is required for FSH release.

Modified form of IGF-1 with an arginine substitution at position 3 and a 13-amino-acid N-terminal extension. These modifications prevent IGF binding protein (IGFBP) sequestration, dramatically increasing bioavailability and potency compared to native IGF-1.

Splice variant of IGF-1 produced in response to mechanical loading (exercise). Activates satellite cells in muscle tissue, promoting myoblast proliferation and muscle repair. Acts locally at the site of muscle damage before being converted to systemic IGF-1.

PEGylated version of mechano growth factor with polyethylene glycol chains attached to extend half-life. Preserves satellite cell activation and muscle repair properties of MGF while allowing systemic rather than purely local administration.

Modified growth hormone releasing hormone (GHRH) analog with amino acid substitutions at positions 2, 8, 15, and 27 to prevent enzymatic degradation. Stimulates pituitary GHRH receptors to amplify natural GH pulses without extending the pulse duration.

Modified GHRH analog conjugated to a Drug Affinity Complex (DAC) that binds serum albumin, dramatically extending half-life. Produces sustained elevation of GH and IGF-1 levels rather than pulsatile release. Continuously stimulates GHRH receptors.

Synthetic hexapeptide GHSR agonist. Stimulates GH release via ghrelin receptor activation on pituitary somatotrophs. Also increases appetite (ghrelin mimetic), cortisol, and prolactin at higher doses. Produces stronger GH pulses than ipamorelin but less selective.

First-generation synthetic hexapeptide GHSR agonist. Potent ghrelin mimetic that stimulates GH release and strongly increases appetite. Also activates the vagus nerve, promoting gastroprotective effects and gastric motility. Less selective than ipamorelin or GHRP-2.

Synthetic hexapeptide GHSR agonist. Produces the strongest acute GH release of all GHRPs. Unique among secretagogues for also activating cardiac protective pathways independent of GH via CD36 scavenger receptor binding.

Selective growth hormone secretagogue receptor (GHSR) agonist. Stimulates pituitary GH release with minimal effect on cortisol, prolactin, or ACTH. One of the most selective ghrelin mimetics available, producing clean GH pulses without appetite stimulation.

Synthetic analog of the first 29 amino acids of endogenous GHRH. Stimulates pituitary somatotrophs to release GH in a physiologic, pulsatile pattern. Preserves negative feedback through somatostatin, preventing supraphysiologic GH levels.

Synthetic GHRH analog with a trans-3-hexenoic acid modification for enhanced stability. Specifically targets visceral adipose tissue reduction via GH-mediated lipolysis. FDA-approved mechanism preserves physiologic GH pulsatility and IGF-1 negative feedback.

Synthetic 11-amino-acid peptide that selectively activates the innate repair receptor (IRR), a heterodimer of EPO receptor and beta common receptor. Promotes tissue protection and repair without erythropoietic effects. Anti-inflammatory via macrophage phenotype switching from M1 to M2.

Endogenous human antimicrobial peptide cleaved from cathelicidin precursor hCAP-18. Disrupts microbial membranes, neutralizes endotoxin (LPS), modulates TLR signaling, promotes wound healing via angiogenesis, and recruits immune cells through chemotactic activity.

Bovine thymus extract containing a mixture of thymic peptide factors. Restores T-cell immunity, promotes thymic regeneration, and modulates immune system homeostasis. Part of the Khavinson bioregulator family targeting the thymus and immune system.

Naturally occurring 28-amino-acid thymic peptide that modulates T-cell maturation and function. Activates toll-like receptors (TLR2, TLR9), promotes dendritic cell maturation, enhances NK cell cytotoxicity, and shifts Th1/Th2 balance toward Th1-dominant immune responses.

AMP-kinase activator that mimics the metabolic effects of exercise. Increases fatty acid oxidation, glucose uptake, and mitochondrial biogenesis through direct AMPK phosphorylation. Shifts cellular metabolism toward an endurance-trained state.

Synthetic tetrapeptide bioregulator that targets cardiac tissue. Promotes cardiomyocyte differentiation, enhances cardiac stem cell activity, and may improve myocardial function by modulating gene expression in heart tissue. Part of the Khavinson bioregulator class.

Synthetic tetrapeptide (Ala-Glu-Asp-Gly) that activates telomerase by inducing the catalytic subunit hTERT. Telomerase elongates telomeres, the protective chromosomal endcaps that shorten with each cell division. May slow cellular aging and extend replicative lifespan.

Mitochondria-derived micropeptide encoded in the 16S rRNA region. Neuroprotective through binding to IGFBP-3 (blocking apoptosis), activating STAT3 signaling, and modulating BAX-mediated cell death. Also improves insulin sensitivity and reduces amyloid-beta toxicity.

Mitochondria-derived peptide encoded by the 12S rRNA gene. Acts as an exercise mimetic by activating AMPK and regulating the folate-methionine cycle. Improves insulin sensitivity, reduces fat accumulation, and enhances cellular stress resistance.

Essential coenzyme present in all living cells. Central to cellular energy metabolism (glycolysis, TCA cycle, oxidative phosphorylation), DNA repair (PARP enzymes), epigenetic regulation (sirtuins), and calcium signaling. Levels decline ~50% between ages 40-60.

Synthetic tripeptide bioregulator that penetrates cell membranes and interacts with DNA in the promoter region of genes involved in neurodifferentiation. Promotes neuronal survival, reduces oxidative stress in brain tissue, and modulates circadian rhythm via pineal gland function.

Mitochondria-targeted tetrapeptide that selectively concentrates in the inner mitochondrial membrane. Binds cardiolipin to optimize electron transport chain function, reduce reactive oxygen species production, and restore mitochondrial bioenergetics.

Synthetic copper-binding tripeptide analog of GHK-Cu with alanine substituted for glycine. Stimulates collagen synthesis and dermal fibroblast proliferation. May offer enhanced stability over GHK-Cu while maintaining copper-dependent tissue remodeling activity.

Pentadecapeptide derived from human gastric juice. Promotes angiogenesis via VEGF upregulation, accelerates tendon and ligament healing, modulates nitric oxide signaling, and protects endothelial cells. Demonstrates systemic healing properties across multiple tissue types.

Naturally occurring copper-binding tripeptide (Gly-His-Lys) complexed with copper(II). Activates tissue remodeling genes, promotes collagen synthesis, increases decorin and glycosaminoglycan production, and recruits stem cells to injury sites. Also suppresses TGF-beta to reduce scarring.

C-terminal tripeptide fragment of alpha-MSH (alpha-melanocyte stimulating hormone). Potent anti-inflammatory that inhibits NF-kB translocation to the nucleus, reducing TNF-alpha, IL-6, and IL-1 beta production. Crosses the blood-brain barrier.

Synthetic analog of thymosin beta-4. Promotes cell migration by sequestering G-actin and upregulating actin polymerization. Reduces inflammation via NF-kB modulation, promotes stem cell differentiation, and accelerates wound healing and tissue repair.

Synthetic analog of endogenous gonadotropin-releasing hormone (GnRH). Pulsatile administration stimulates FSH and LH release from the anterior pituitary. Continuous administration paradoxically downregulates the HPG axis through receptor desensitization.

Glycoprotein hormone that mimics luteinizing hormone (LH) action. In males, stimulates Leydig cells to produce testosterone. In females, triggers ovulation and supports corpus luteum progesterone production. Maintains testicular function during exogenous hormone use.

Combination of FSH and LH extracted from post-menopausal urine. Directly stimulates ovarian follicular development (FSH component) and supports ovulation and corpus luteum function (LH component). Used in assisted reproduction protocols.

C-terminal decapeptide fragment of kisspeptin that activates GPR54 (KISS1R) receptors on GnRH neurons. Potently stimulates the hypothalamic-pituitary-gonadal (HPG) axis, triggering pulsatile GnRH release and downstream LH and FSH secretion.

Nine-amino-acid neuropeptide hormone produced in the hypothalamus. Promotes pair bonding, social trust, empathy, and orgasm. Stimulates uterine contractions and milk letdown. Modulates anxiety, stress response, and social cognition through widespread CNS receptor distribution.

Melanocortin-4 receptor (MC4R) agonist derived from Melanotan II. Acts centrally in the hypothalamus to increase sexual desire and arousal through dopaminergic pathways. Unlike PDE5 inhibitors, works on desire rather than mechanical erectile function.

Potent GnRH agonist with greatly enhanced receptor binding affinity. Initial administration causes a flare of LH/FSH and testosterone. Continuous administration leads to profound suppression of the HPG axis via pituitary GnRH receptor downregulation.

Small molecule inhibitor of NNMT. Increases cellular NAD+ and SAM levels, activating SIRT1-dependent energy expenditure pathways.

Modified fragment of human growth hormone (amino acids 177-191). Stimulates lipolysis and inhibits lipogenesis without growth-promoting or diabetogenic effects.

Long-acting amylin analog that slows gastric emptying, promotes satiety, and reduces postprandial glucagon secretion. Works synergistically with GLP-1 agonists.

Fixed-dose combination of cagrilintide (amylin analog) and semaglutide (GLP-1 agonist). Targets three distinct appetite and metabolic pathways simultaneously.

GLP-1 receptor agonist fused to a modified IgG4 Fc fragment for extended duration. Weekly dosing improves compliance.

The lipolytic fragment of human growth hormone encompassing amino acids 176-191. Promotes fat metabolism through beta-3 adrenergic receptor pathways.

Injectable fat-dissolving solution containing riboflavin, lecithin, and bromelain. Disrupts adipocyte cell membranes.

GLP-1 receptor agonist with 97% homology to native GLP-1. Enhances glucose-dependent insulin secretion, suppresses glucagon, slows gastric emptying.

Dual GLP-1/glucagon receptor agonist. Promotes direct hepatic fat oxidation and thermogenesis alongside appetite suppression.

Triple agonist targeting GIP, GLP-1, and glucagon receptors simultaneously. The glucagon receptor activation increases energy expenditure and hepatic fat oxidation.

GLP-1 receptor agonist that mimics incretin hormones. Enhances insulin secretion in a glucose-dependent manner, suppresses glucagon release, and slows gastric emptying. Centrally reduces appetite through hypothalamic signaling.

ERRa agonist that mimics the transcriptional effects of exercise. Activates mitochondrial biogenesis and oxidative metabolism pathways.

Dual GLP-1/glucagon receptor agonist. Glucagon component drives energy expenditure and hepatic lipid metabolism. Shows promise for MASH.

Dual GIP/GLP-1 receptor agonist. Activates both glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 receptors simultaneously. Produces greater weight loss and glycemic control than single-receptor agonists.