Biological Pathways
14 pathways covering signaling cascades, receptor interactions, and molecular mechanisms affected by peptide compounds.
AMPK Pathway
Angiogenesis Pathways
How injury and hypoxia coordinate endothelial sprouting, matrix remodeling, perfusion, and vessel maturation—and where peptide research intersects with that network.
Ghrelin / GHSR-1a Signaling
The ghrelin/GHSR-1a pathway links a stomach-derived acylated peptide to a constitutively active Class A GPCR that governs pulsatile growth hormone secretion, appetite, energy metabolism, and reward circuitry. Ipamorelin and hexarelin are selective synthetic agonists at GHSR-1a; CJC-1295 engages the parallel GHRH receptor pathway to amplify the same somatotroph output.
Growth Hormone Receptor
IGF-1 / JAK2-STAT5 Signaling Axis
The IGF-1 / JAK2-STAT5 axis begins with ligand binding at the IGF-1 receptor (IGF1R), a heterotetrameric receptor tyrosine kinase, and propagates through IRS-1/2 adapter proteins into the PI3K/AKT/mTOR and MAPK/ERK cascades. A parallel JAK2-STAT5 arm drives transcription of growth and metabolic genes. Together these branches control somatic growth, skeletal muscle accretion, adipose tissue lipolysis, glucose metabolism, and cell survival. IGF-1 LR3 is a long-acting IGF-1 analog that activates IGF1R directly; sermorelin, tesamorelin, and CJC-1295 engage the upstream GH axis that governs endogenous IGF-1 production.
Incretin Axis (GLP-1, GIP)
The incretin axis is a gut-to-pancreas hormonal circuit in which meal-stimulated GLP-1 from intestinal L-cells and GIP from K-cells potentiate glucose-dependent insulin secretion through their respective class B1 GPCRs. Both receptors couple to Gs, elevate cAMP, and activate PKA and Epac2 to amplify KATP channel closure and calcium-dependent exocytosis in beta cells. Semaglutide, tirzepatide, and retatrutide each target this axis with increasing receptor breadth.
MAPK Cascade
Mitochondrial Biogenesis
mTOR Signaling
Neuropeptides & Cognitive Function
The neuropeptide cognitive signaling pathway links a family of short regulatory peptides to core plasticity and neuroinhibitory machinery in the hippocampus, prefrontal cortex, and brainstem. Semax (an ACTH 4-10 analogue) engages melanocortin MC4R to drive cAMP/PKA/CREB-mediated BDNF transcription and TrkB-dependent synaptic plasticity. Selank (a tuftsin analogue) allosterically modulates GABA-A receptors, suppresses orexin signaling, inhibits enkephalin-degrading enzymes, and elevates hippocampal BDNF. DSIP (delta sleep-inducing peptide) potentiates GABAergic inhibition, blocks NMDA receptor currents, suppresses HPA-axis ACTH output, and stimulates calcium-dependent Met-enkephalin release. All three converge on CREB phosphorylation, BDNF/TrkB activation, and downstream MAPK/ERK and PI3K/Akt effectors that govern long-term potentiation, memory consolidation, and neuronal survival.