Peptide Profiles
Peptide Profiles
GLP-1 · Growth Hormone · Inflammatory · Mitochondrial · Angiogenesis
Comprehensive research profiles for every peptide in our catalogue. Each entry covers molecular classification, mechanism of action, primary research applications, key molecular targets, and storage requirements — everything needed to understand a compound before designing a study.
GLP-1 & Metabolic Peptides
Incretin agonists · dual and triple receptor compounds · metabolic pathway research
Semaglutide is a GLP-1 receptor agonist modified with a C-18 fatty acid side chain that enables reversible albumin binding, dramatically extending its circulating half-life. It activates GLP-1 receptors on pancreatic β-cells to stimulate glucose-dependent insulin secretion, suppresses glucagon release from α-cells, delays gastric emptying, and modulates hypothalamic appetite pathways via POMC neuron activation.
- Glucose-dependent insulin secretion and β-cell function studies
- Hypothalamic appetite and satiety pathway research
- Cardiovascular outcome and cardiometabolic risk research
- Hepatic steatosis and NASH preclinical models
- Neuroprotection and CNS GLP-1 receptor studies
- Oral vs injectable bioavailability and ADME research
Tirzepatide is a synthetic peptide designed as a dual agonist of both GLP-1 and GIP receptors. Simultaneous activation of both incretin pathways produces synergistic enhancement of glucose-dependent insulin secretion, superior β-cell preservation, GIP-mediated adipose tissue lipolysis, and greater weight reduction than single-receptor approaches. It also modulates brown adipose tissue thermogenesis and central appetite signalling.
- Dual incretin pathway synergy and signal integration studies
- GIP receptor function and adipose tissue metabolism research
- Comparative efficacy vs GLP-1 mono-agonism protocols
- Brown adipose tissue activation and thermogenesis studies
- Superior glycaemic control mechanism investigation
- β-cell preservation and insulin resistance research models
Retatrutide simultaneously activates GLP-1, GIP, and glucagon receptors — the first triple incretin agonist in research. The addition of glucagon receptor co-activation significantly amplifies energy expenditure through hepatic glucose regulation and thermogenic pathway stimulation, producing metabolic effects beyond those achievable with dual agonism. Early models suggest unprecedented weight reduction potential exceeding 20% in preclinical studies.
- Triple receptor synergy and signal integration research
- Glucagon receptor contribution to energy expenditure studies
- Enhanced thermogenesis and brown adipose tissue activation
- Hepatic gluconeogenesis and lipid metabolism research
- Comparison with mono- and dual-agonist compounds
- NASH and severe obesity preclinical research models
Growth Hormone Peptides
GHRH analogues · GH releasing peptides · IGF-1 axis · somatotropic research
CJC-1295 is a GHRH analogue modified with Drug Affinity Complex (DAC) technology that enables reversible covalent bonding to circulating albumin, creating a natural peptide depot. Active CJC-1295 is released slowly over 6–8 days, providing sustained stimulation of pituitary GHRH receptors and pulsatile growth hormone release, followed by hepatic IGF-1 production. Feedback regulation via somatostatin is preserved.
- Sustained GH elevation and chronic somatotropic axis stimulation
- Age-related GH decline and somatopause research models
- IGF-1 dose-response and biomarker profiling studies
- Albumin binding kinetics and extended-release PK research
- Body composition: lean mass and adipose tissue studies
- Combination protocols with Ipamorelin for synergistic GH release
Ipamorelin is a pentapeptide that selectively binds and activates ghrelin receptors (GHS-R1a) in pituitary somatotrophs via Gq/G11 protein coupling and PLC/IP3/DAG-mediated calcium mobilisation. Its defining characteristic is exceptional receptor selectivity — it stimulates discrete, physiological-amplitude GH pulses without meaningfully elevating cortisol, prolactin, or ACTH, making it the preferred tool for studies requiring isolated GH data.
- Isolated GH pulse research free from confounding hormonal changes
- GHS-R1a subtype selectivity and receptor desensitisation studies
- Paediatric growth, elderly somatopause, and gender-specific GH research
- Pituitary responsiveness and GH pulse amplitude studies
- Synergistic combination with CJC-1295 for dual-pathway stimulation
- Long-duration and sensitive research model tolerability studies
IGF-1 LR3 is a recombinant analogue of IGF-1 with an N-terminal arginine extension and Glu3→Arg3 substitution that reduces IGF-binding protein (IGFBP) affinity by over 1,000-fold. This dramatically extends its active half-life versus native IGF-1. It directly activates IGF-1 receptors in peripheral tissues, triggering IRS-1/2 phosphorylation and downstream PI3K/Akt survival and MAPK/ERK proliferative signalling, bypassing pituitary axis control entirely.
- Skeletal muscle satellite cell activation and protein synthesis studies
- Neuroprotection, neurogenesis, and neurodegenerative disease models
- PI3K/Akt and MAPK/ERK anabolic signalling pathway research
- Direct IGF-1R studies independent of pituitary GH axis
- Muscle wasting, sarcopaenia, and bone density research models
- Cell proliferation, apoptosis, and stem cell differentiation studies
Sermorelin is the synthetic 29-amino acid N-terminal fragment of endogenous GHRH — the minimum sequence required for full GHRH receptor binding and somatotroph stimulation. It preserves the natural feedback architecture of the hypothalamic-pituitary axis, producing physiological GH pulses modulated by endogenous somatostatin. Its short half-life and well-characterised response kinetics make it the gold standard reference compound for GH stimulation testing.
- GH deficiency stimulation testing and pituitary reserve assessment
- Hypothalamic-pituitary axis physiology and feedback regulation research
- Age-related somatopause and GH decline longitudinal studies
- Circadian rhythm, sleep architecture, and nocturnal GH pulse research
- Reference standard for comparative GH secretagogue studies
- Paediatric growth research and diagnostic stimulation protocols
Tesamorelin is GHRH(1-44) conjugated with trans-3-hexenoic acid, which confers resistance to DPP-IV cleavage, extending its activity window. GH released in response to Tesamorelin activates hormone-sensitive lipase in visceral adipose tissue depots specifically, producing selective visceral fat reduction while preserving lean mass. This regional selectivity distinguishes it from other GH secretagogues and makes it uniquely valuable for lipodystrophy and metabolic syndrome research.
- Visceral adipose tissue biology and regional fat distribution research
- HIV-associated lipodystrophy and metabolic syndrome models
- Hormone-sensitive lipase activation and GH-mediated lipolysis
- Cardiovascular risk marker research in metabolic disease models
- Hippocampal IGF-1 upregulation and cognitive function studies
- Adipokine regulation and lipid metabolism research
Inflammatory Signalling Peptides
Immune modulators · tissue repair compounds · cytokine regulation research
Thymosin Alpha-1 (Tα1) is a 28-amino acid peptide originally isolated from thymosin fraction 5 of the thymus gland. It activates TLR2 and TLR9 signalling to enhance innate immune pattern recognition, promotes T-cell maturation and Th1/Th2 balance, stimulates dendritic cell antigen-presenting capacity, enhances NK cell and CTL cytotoxic activity, and modulates regulatory T-cell function. It optimises cytokine production — upregulating IL-2 and IFN-γ while supporting IL-10 anti-inflammatory balance.
- T-cell maturation, Th1/Th2 balance, and adaptive immunity studies
- Immunosenescence and thymic involution in ageing research models
- NK cell and CTL cytotoxic activity enhancement research
- Vaccine response enhancement and immune restoration studies
- Sepsis, immunodeficiency, and chronic infection research models
- Cancer immunotherapy optimisation and immune checkpoint research
KPV is the bioactive C-terminal tripeptide of α-melanocyte stimulating hormone, retaining the parent molecule's anti-inflammatory potency with improved stability. It acts as a MC1R and MC3R agonist, suppressing NF-κB nuclear translocation and downstream pro-inflammatory gene expression. Crucially, KPV is transported across intestinal epithelial cells by the PepT1 oligopeptide transporter, enabling direct intracellular anti-inflammatory action independent of surface receptor binding.
- Melanocortin receptor (MC1R/MC3R) pathway and NF-κB inhibition research
- Inflammatory bowel disease and colitis preclinical models
- PepT1 transporter-mediated intestinal cell uptake studies
- Skin inflammation, dermatitis, and topical anti-inflammatory research
- Neuroinflammation and blood-brain barrier protection studies
- Cytokine modulation (TNF-α, IL-1β, IL-6 reduction) research
BPC-157 is a 15-amino acid synthetic peptide derived from a sequence in human gastric juice. Its research profile spans multiple organ systems: it activates FAK and paxillin phosphorylation to promote fibroblast migration for tendon and tissue repair; upregulates VEGFR2 and eNOS for vascular protection and neovascularisation; modulates COX-2 and NF-κB to reduce inflammatory cascades; and upregulates BDNF and dopamine pathway components for neuroprotective effects.
- Tendon, ligament, and musculoskeletal tissue repair research
- Gastrointestinal protection and gut-brain axis signalling studies
- VEGF-mediated angiogenesis and wound vascularisation research
- Neuroprotection, BDNF upregulation, and CNS injury models
- Anti-inflammatory cytokine balance and NF-κB pathway studies
- Bone healing, fracture repair, and orthopaedic research models
TB-500 is the seven-amino acid active fragment of Thymosin Beta-4 containing the conserved actin-binding domain LKKTETQ. By sequestering G-actin monomers, it regulates the dynamic equilibrium between G-actin and F-actin, facilitating lamellipodia formation and directed cell migration. It activates ILK (integrin-linked kinase) for cell survival signalling, suppresses NF-κB-mediated inflammation, and stimulates cardiac progenitor cell mobilisation and pericyte recruitment for vascular maturation.
- G-actin sequestration and cytoskeletal dynamics research
- Wound closure, keratinocyte migration, and skin repair studies
- Cardiac progenitor cell activation and myocardial repair models
- Anti-fibrotic and anti-inflammatory mechanism studies
- Endothelial cell tube formation and angiogenesis research
- Tendon, muscle, and ligament regeneration in vivo models
Mitochondrial & Bioenergetics Compounds
Mitochondrial-derived peptides · NAD+ precursors · cellular energy metabolism research
MOTS-c is encoded within the mitochondrial 12S rRNA gene — one of the few known peptides of mitochondrial genomic origin. Under metabolic stress, it translocates from the cytoplasm to the nucleus, acting as a retrograde mitochondrial signal that regulates nuclear gene expression. It suppresses the folate cycle, generating AICAR to activate AMPK, which promotes GLUT4 translocation, glucose uptake, and mitochondrial biogenesis — replicating key molecular signatures of endurance exercise.
- Mitochondrial retrograde nuclear signalling and gene regulation
- AMPK activation, glucose uptake, and insulin sensitivity research
- Exercise mimetic metabolic adaptation studies
- Ageing, longevity, and mitochondrial decline research models
- Folate cycle–AICAR axis suppression mechanism studies
- MOTS-c as circulating biomarker in ageing and centenarian research
NMN is a direct NAD+ biosynthesis intermediate entering cells via the Slc12a8 transporter to rapidly raise intracellular NAD+ levels. Elevated NAD+ activates sirtuins (SIRT1–SIRT7) — NAD+-dependent deacetylases that regulate mitochondrial biogenesis via PGC-1α, DNA damage repair via PARP-1, circadian rhythm via CLOCK/BMAL1, and cellular stress resistance via multiple downstream targets. NAD+ declines 50%+ in key tissues in animal ageing models, positioning NMN as a central ageing biology tool.
- NAD+ repletion and sirtuin activation in ageing models
- Mitochondrial biogenesis via PGC-1α and NRF2 pathway studies
- DNA repair (PARP-1/PARP-2) and genomic stability research
- Neurodegeneration, cognitive decline, and hippocampal NAD+ studies
- Circadian clock regulation and CLOCK/BMAL1 pathway research
- Skeletal muscle endurance and metabolic efficiency studies
Nicotinamide Riboside (NR) enters cells via equilibrative nucleoside transporters (ENTs) and is phosphorylated to NMN then NAD+ via NRK1/NRK2 kinases — an alternative biosynthesis route to the NAMPT pathway used by NMN. NR preferentially elevates NAD+ in tissues with high NRK expression such as muscle and liver, activating sirtuins, supporting mitochondrial respiratory capacity, and restoring NAD+/NADH redox balance. Its distinct cellular uptake mechanism makes it a complementary research tool to NMN for pathway dissection.
- NRK kinase pathway vs NAMPT pathway NAD+ biosynthesis comparison
- Mitochondrial respiratory capacity and ETC function studies
- Muscle function, endurance, and exercise performance research models
- Liver health, NAFLD, and hepatic NAD+ metabolism studies
- Neuroprotection and cognitive function in ageing models
- Immune system ageing and stem cell function research
Angiogenesis & Vascular Biology Peptides
Endothelial biology · vessel formation · matrix remodelling · wound vascularisation
GHK-Cu is an endogenous human plasma tripeptide with high-affinity copper chelation. It delivers bioavailable copper to lysyl oxidase for collagen and elastin crosslinking maturation, activates matrix metalloproteinases (MMP-1, MMP-2, MMP-9) for extracellular matrix remodelling, upregulates VEGF and FGF expression to promote endothelial proliferation and angiogenesis, and activates antioxidant enzymes SOD and catalase at wound sites. It also upregulates neurotrophins BDNF and NGF in neural repair contexts.
- Copper-dependent collagen crosslinking and ECM remodelling research
- VEGF/FGF-mediated angiogenesis and endothelial proliferation studies
- Skin wound healing, dermal collagen density, and elasticity research
- Hair follicle vascularisation and follicle biology studies
- SOD/catalase antioxidant enzyme activation at wound sites
- Age-related vascular decline and skin senescence research models
In the context of vascular biology, BPC-157 upregulates VEGFR2 expression on endothelial cells, stimulating sprouting and tube formation in ischaemia and wound models. eNOS-mediated nitric oxide production contributes to vasodilatory responses and endothelial protection. In vivo studies demonstrate accelerated wound closure with measurably increased capillary density at wound sites, ischaemia-reperfusion injury protection, and enhanced tendon-to-bone healing through concurrent vascularisation and collagen maturation.
- VEGFR2 upregulation and endothelial sprouting in ischaemia models
- eNOS-mediated nitric oxide production and vasoprotection studies
- Wound capillary density quantification and healing rate research
- Ischaemia-reperfusion injury protection mechanism studies
- Tendon-to-bone vascular healing and repair research
- Gastrointestinal mucosal vascularisation studies
TB-500's G-actin sequestration activity is directly relevant to angiogenesis: endothelial cell migration and tube formation depend critically on cytoskeletal actin dynamics. By enabling lamellipodia formation, TB-500 facilitates directed endothelial sprouting. ILK pathway activation supports pericyte recruitment to nascent vessels for vascular maturation. In cardiac models, it mobilises progenitor cells for vasculogenesis. Limb ischaemia models demonstrate collateral vessel development and improved tissue perfusion.
- G-actin/lamellipodia-driven endothelial cell migration and sprouting
- Matrigel tube formation and in vitro angiogenesis assays
- Pericyte recruitment and nascent vessel stabilisation studies
- Cardiac vasculogenesis and progenitor cell mobilisation research
- Limb ischaemia collateral vessel development and perfusion studies
- ILK pathway activation and vascular survival signalling
More Than Just Profiles
Each peptide profile connects to detailed mechanism guides, protocol frameworks, comparison tables, and research summaries — everything needed to design credible studies with these compounds.
Mechanism Guides
Step-by-step signalling cascade maps and molecular pathway diagrams for every compound category
Research Summaries
Evidence-based overviews of primary research findings, key studies, and current investigational directions
Protocol Frameworks
In vitro, in vivo, and analytical protocol guidance including working concentrations and biomarker selection
Every Profile Backed by
Independent Verification
All compounds in our catalogue are tested to ≥98% HPLC purity by accredited third-party laboratories. Certificates of Analysis available on request for every batch.