Peptide Reference
Library

Mimics the fat-burning region of hGH without anabolic effects; stimulates lipolysis in adipocytes.

Upregulates growth factor expression (VEGF, FGF), promotes angiogenesis and tendon-to-bone healing.

Contains neurotrophic factors (BDNF, CNTF, GDNF analogs) that promote neurogenesis, synaptogenesis, and neuronal survival.

Binds GHRH receptors to stimulate natural pulsatile GH secretion without desensitization.

Binds to GHRH receptors on pituitary somatotrophs, stimulating pulsatile GH release.

Binds hepatocyte growth factor (HGF) receptor to promote spinogenesis and synaptogenesis.

Crosses blood-brain barrier; induces delta-wave sleep, modulates HPA axis.

Activates telomerase in somatic cells, potentially extending Hayflick limit.

Binds and neutralizes myostatin (GDF-8) and activins, removing the natural "brake" on muscle growth. Also modulates FSH levels.

Disrupts FOXO4-p53 interaction in senescent cells, releasing p53 to trigger apoptosis. The D-retro-inverso structure provides protease resistance.

Stimulates collagen synthesis, glycosaminoglycans, and decorin; promotes wound repair and anti-inflammatory effects.

Ghrelin receptor agonist; more potent GH release vs GHRP-6 with moderate cortisol/prolactin increase.

Ghrelin mimetic activating GHS-R1a receptor on pituitary somatotrophs.

GHK-Cu stimulates collagen/elastin synthesis via decorin upregulation; BPC-157 promotes VEGF-driven angiogenesis and fibroblast migration; TB-500 (Thymosin Beta-4 fragment) promotes actin polymerization and systemic cell migration for diffuse tissue repair.

Neutralizes reactive oxygen species (ROS), regenerates vitamins C and E, conjugates toxins for excretion, supports T-cell proliferation.

Pulsatile stimulation of anterior pituitary gland to release LH and FSH, maintaining gonadal function during exogenous hormone use.

Ghrelin receptor agonist; strongest GH release of GHRPs but desensitization occurs at ~4 weeks.

Stimulates lipolysis and inhibits lipogenesis in adipocytes without affecting blood glucose or IGF-1 levels.

Binds IGFBP-3 and BAX to inhibit apoptosis; activates STAT3 signaling; neuroprotective against beta-amyloid toxicity.

Activates IGF-1 receptors to promote muscle hypertrophy, cell proliferation, and protein synthesis. LR3 modification reduces IGFBP binding.

Ghrelin receptor agonist with high selectivity for GH release.

Activates GPR54 (KISS1R) receptor on hypothalamic GnRH neurons, triggering pulsatile GnRH release and downstream LH/FSH secretion.

All GLOW mechanisms plus: KPV blocks NF-κB signaling to suppress TNF-α, IL-6, IL-1β production, creating an anti-inflammatory environment that maximizes BPC-157 and TB-500 tissue repair activity.

Inhibits NF-κB signaling pathway, reducing pro-inflammatory cytokine production (TNF-α, IL-6, IL-1β). Effective systemically, topically, and orally.

Disrupts bacterial membranes; modulates immune response via TLR signaling and chemotaxis.

Activates MC1R (melanocyte stimulation), MC3R/MC4R (sexual arousal, appetite).

Activates muscle satellite cells at the injury site; extremely short half-life requires local injection for targeted repair.

Oral ghrelin receptor agonist; raises GH/IGF-1 without suppressing natural secretion.

Activates AMPK pathway; regulates mitochondrial metabolism and glucose uptake.

Serves as electron carrier in mitochondrial electron transport chain; activates sirtuins (SIRT1-7) for DNA repair and gene silencing; substrate for PARPs.

Binds oxytocin receptors in brain and peripheral tissues; modulates social behavior, anxiety, and stress response via hypothalamic-pituitary axis.

Activates satellite cells for muscle repair; PEG modification extends systemic half-life from minutes to days.

Penetrates nuclear membrane and binds DNA, regulating gene expression in neuronal cells. Promotes neuroprotection, reduces oxidative stress in brain tissue, and normalizes pineal gland melatonin production.

Activates melanocortin-4 receptors in the CNS to enhance sexual arousal.

Activates GLP-1, GIP, and glucagon receptors simultaneously for superior metabolic effects.

Modulates GABA, serotonin, dopamine, and norepinephrine systems; enhances BDNF expression.

Mimics incretin GLP-1, stimulates insulin secretion, suppresses glucagon, slows gastric emptying, reduces appetite.

Increases BDNF/NGF, modulates serotonergic system; neuroprotective against oxidative stress.

Stimulates pituitary somatotrophs to release GH in a pulsatile, physiological pattern. Does not suppress endogenous GH production.

Synergistic GH release: GHRH analog (Sermorelin) amplifies pulse amplitude at pituitary, while GHRP (Ipamorelin) initiates pulse via ghrelin receptor. Combined output exceeds either alone by 2-5×.

Binds cardiolipin on inner mitochondrial membrane, stabilizing electron transport chain.

Promotes actin polymerization, cell migration, and new blood vessel formation.

Synthetic GHRH(1-44) that stimulates pulsatile GH release from pituitary.

Restores thymic function and T-cell differentiation in aging immune systems; modulates cytokine production and immune homeostasis.

Activates toll-like receptors, enhances dendritic cell function, stimulates T-cell maturation and NK cell activity.

Dual incretin agonist activating both GIP and GLP-1 receptors for enhanced glycemic control and weight loss.

Initial GnRH receptor stimulation causes LH/FSH surge; single low-dose use (100 mcg) can restart HPTA axis after suppression.

Modulates immune response via VPAC1/VPAC2 receptors; reduces pulmonary inflammation; neuroprotective and vasodilatory.