Peptides Reference

Adipotide links an adipose-vasculature homing sequence to a pro-apoptotic motif.

It is derived from the C-terminal region of hGH and is proposed to influence lipolysis and inhibit lipogenesis, with less impact on IGF-1 signaling than full-length growth hormone.

Proposed mechanisms include angiogenesis-related signaling, nitric-oxide pathway modulation, fibroblast migration, and cytoskeletal repair signaling.

The blend concept aims to combine BPC-157’s healing and vascular-repair signaling with TB-500’s cell migration, cytoskeletal, and angiogenesis-related biology.

The combination is intended to pair BPC-157’s vascular-repair and fibroblast-signaling hypotheses with TB-500’s cell-migration and tissue-remodeling effects.

CJC-1295 aims to stimulate GHRH receptor signaling at the pituitary, while ipamorelin acts at the ghrelin receptor to augment pulsatile GH secretion.

DSIP has been proposed to interact with sleep architecture, circadian regulation, and stress-response pathways, but its exact physiologic role remains controversial.

The core hypothesis is that epithalon influences telomerase activity and downstream markers of cellular senescence.

Its proposed actions include support of collagen synthesis, extracellular-matrix remodeling, and wound-healing signaling.

The blend attempts to unite collagen and extracellular-matrix biology from GHK-Cu with angiogenesis, fibroblast, and cell-migration hypotheses associated with BPC-157 and TB-500.

Hexarelin acts through the ghrelin receptor pathway to stimulate GH secretion.

The fragment is proposed to influence lipolysis and adipose metabolism without reproducing the full anabolic, glycemic, and IGF-1-mediated physiology of somatropin.

It is intended to engage IGF-1 receptor signaling, promoting anabolic and metabolic effects relevant to protein synthesis, muscle growth, and tissue adaptation.

It acts at the ghrelin receptor to stimulate pulsatile GH release.

KPV is proposed to modulate inflammatory signaling, including NF-kB-related pathways, and to reduce mucosal injury in inflammatory models.

LL-37 disrupts microbial membranes and also participates in immune signaling, inflammation, and tissue-repair responses.

Proposed mechanisms include AMPK-related signaling, mitochondrial stress adaptation, and broader regulation of metabolic homeostasis.

NAD+ supports core redox reactions, mitochondrial energy production, and sirtuin-associated stress-response pathways.

Oxytocin acts through oxytocin receptors in the brain and peripheral tissues, influencing social salience, bonding, emotional processing, and reproductive biology.

It acts as a melanocortin receptor agonist, influencing central pathways involved in sexual desire and arousal rather than acting through vasodilation like PDE5 inhibitors.

It combines incretin signaling with glucagon-pathway activation, aiming to enhance appetite suppression, metabolic regulation, and energy expenditure.

Proposed mechanisms include modulation of GABAergic tone, serotonin-related pathways, stress-response systems, and gene expression related to neurotransmission.

The blend concept relies on complementary neurochemical hypotheses: semax for BDNF-related and neuroprotective effects, and selank for GABA-, serotonin-, and stress-related modulation.

Semaglutide mimics GLP-1 signaling to slow gastric emptying, reduce appetite, improve glucose regulation, and influence central satiety pathways.

Proposed mechanisms include BDNF-related signaling, neuroinflammation modulation, and support of neuronal survival under ischemic or stress conditions.

It activates the pituitary GHRH receptor to stimulate endogenous GH release.

Somatropin directly activates growth-hormone receptors, influencing IGF-1 production, body composition, metabolic regulation, and tissue growth pathways.

The scientific rationale centers on actin-binding and cytoskeletal regulation, cell migration, angiogenesis, and tissue remodeling.

As a GHRH analog, tesamorelin stimulates endogenous GH release and increases IGF-1 exposure.

It is associated with T-cell activation, dendritic-cell function, and broader modulation of innate and adaptive immune signaling.

It activates both GIP and GLP-1 pathways to improve glycemic control, suppress appetite, reduce caloric intake, and meaningfully lower body weight.

Activates the ghrelin receptor to increase endogenous GH secretion and raise IGF-1.

Linked to experimental serotonergic and stress-response signaling in preclinical models.

Linked to neuronal gene-regulation and protective signaling in aging-brain models.

Linked to mitochondrial respiration and metabolic-expenditure signaling in preclinical models.

Targets mitochondrial function, oxidative stress, and ATP-efficiency pathways.

Inhibits monoamine reuptake to reduce appetite and support weight loss.

Linked to actin regulation, cell migration, angiogenesis, and tissue remodeling.

Activates melanocortin receptors involved in pigmentation and central neuroendocrine signaling.