Category
Pain & Inflammation
Peptides studied for their effects on inflammatory signaling cascades, analgesic pathways, and conditions where chronic inflammation drives tissue damage. BPC-157 and KPV operate through distinct mechanisms but both show consistent anti-inflammatory effects across multiple research models.
9 peptides in this category
How do anti-inflammatory peptides work?
Anti-inflammatory peptides work through several distinct mechanisms. BPC-157 suppresses NF-kB activation and modulates nitric oxide signaling, reducing pro-inflammatory cytokine production in multiple tissues without broadly suppressing immune function. KPV binds melanocortin receptors on immune cells and intestinal epithelium to dampen cytokine secretion specifically in gut inflammation. Ziconotide blocks calcium channels in spinal pain neurons, providing analgesia through a non-opioid mechanism. Unlike NSAIDs, most peptide-based approaches target specific inflammatory nodes rather than systemically suppressing prostaglandin synthesis.
Inflammation is not a single process but a coordinated cascade involving pattern recognition, cytokine release, immune cell recruitment, arachidonic acid metabolism, and resolution signaling. Therapeutic peptides in this category target specific nodes in that cascade rather than broadly suppressing the entire system, which is one potential advantage over NSAIDs or corticosteroids. BPC-157 appears to work primarily through nitric oxide pathway modulation and direct inhibition of NF-kB activation, the transcription factor that controls expression of most pro-inflammatory cytokines including TNF-alpha, IL-1beta, and IL-6. This translates to reduced inflammation in multiple organ systems — gut, tendon, brain, and muscle — across a wide range of insult models.
KPV (Lys-Pro-Val) is an alpha-MSH tripeptide that binds melanocortin receptors on macrophages and intestinal epithelial cells, reducing pro-inflammatory cytokine secretion and NF-kB nuclear translocation. It has been studied particularly in gut inflammation models. Other peptides in this category include spadin (a natriuretic peptide prohormone fragment with antidepressant-adjacent analgesic properties) and ziconotide, a synthetic version of omega-conotoxin from cone snail venom — the only peptide-based intrathecal analgesic currently in clinical use for severe chronic pain.
Compounds
Peptides in this category
BPC-157
PreclinicalBody Protection Compound 157 · PL 14736
BPC-157 is a 15-amino-acid peptide fragment derived from human gastric juice. It is one of the most extensively researched peptides for tissue repair, demonstrating accelerated healing of tendons, ligaments, muscle, bone, and gut lining in animal models. It appears to upregulate growth hormone receptors and promote angiogenesis at injury sites.
C₆₂H₉₈N₁₆O₂₂ · 1419.55 Da
Bradykinin
PreclinicalBK · Kallidin precursor fragment
Bradykinin is a 9-amino-acid vasoactive peptide of the kinin-kallikrein system. It produces vasodilation, increased vascular permeability, pain, and inflammation by acting on B1 and B2 receptors. ACE inhibitors (a major drug class) lower blood pressure partly by preventing bradykinin degradation. Icatibant, a B2 antagonist, is approved for hereditary angioedema. Research also implicates bradykinin in COVID-19 pathology (bradykinin storm hypothesis).
Enkephalins
PreclinicalLeu-Enkephalin · Met-Enkephalin
Enkephalins are endogenous opioid pentapeptides (Met-enkephalin and Leu-enkephalin) acting as natural ligands for delta and mu opioid receptors. They modulate pain, mood, reward, and immune function. Low-dose naltrexone (LDN) works partly by transiently blocking opioid receptors to upregulate enkephalin production. Methionine enkephalin (met-enkephalin) has shown immune-modulating and anti-tumor properties in research, particularly for HIV and cancer.
Galanin
PreclinicalGAL
Galanin is a 29-30 amino acid neuropeptide widely distributed throughout the CNS and peripheral nervous system. It modulates memory, mood, pain, seizures, appetite, and sleep via three receptor subtypes (GALR1–3). Research focuses on its roles in Alzheimer's disease (galanin hyperinnervation of cholinergic neurons), depression, epilepsy, and eating behavior. Both agonists and antagonists have therapeutic potential depending on the target condition.
KPV
PreclinicalLys-Pro-Val · α-MSH C-terminal tripeptide
KPV is a tripeptide derived from the C-terminal sequence of alpha-melanocyte-stimulating hormone (α-MSH). It exhibits potent anti-inflammatory effects by inhibiting NF-κB signaling and proinflammatory cytokine production. Research is particularly focused on its potential for inflammatory bowel disease, colitis, and skin inflammation, with studies showing efficacy even when administered orally or topically.
Neurotensin
PreclinicalNT · NTS
Neurotensin is a 13-amino-acid neuropeptide found in the brain and GI tract. Centrally, it modulates dopamine circuits, acts as an endogenous antipsychotic-like agent, and is analgesic. Peripherally, it inhibits gastric acid secretion, stimulates pancreatic secretion, and promotes fat absorption. Research explores neurotensin analogs for pain, schizophrenia, Parkinson's disease, and metabolic regulation.
Substance P
PreclinicalSP · NK1 ligand
Substance P is an 11-amino-acid neuropeptide of the tachykinin family and a primary neurotransmitter of pain signaling in the spinal cord. It binds NK1 receptors to mediate neurogenic inflammation, pain hypersensitivity, and emotional processing. NK1 antagonists have been developed for pain, depression (aprepitant), and nausea. Research also implicates substance P in wound healing, immune activation, and neuroinflammation.
VIP
Phase IIVasoactive Intestinal Peptide · Vasoactive Intestinal Polypeptide
VIP (Vasoactive Intestinal Peptide) is a 28-amino-acid neuropeptide with pleiotropic anti-inflammatory, bronchodilatory, and immunomodulatory effects mediated through VPAC1 and VPAC2 receptors. Research spans pulmonary arterial hypertension (inhaled VIP trials), inflammatory bowel disease, sepsis, Parkinson's disease, and CIRS (chronic inflammatory response syndrome). It suppresses Th1 cytokines and promotes Treg cell function.
α-MSH
PreclinicalAlpha-Melanocyte-Stimulating Hormone · α-Melanotropin
α-MSH is an endogenous 13-amino-acid peptide derived from POMC (pro-opiomelanocortin). It activates MC1R to stimulate melanin production in skin, MC4R to suppress appetite and regulate energy expenditure, and MC3R/MC1R to exert potent anti-inflammatory effects. It is the parent compound from which many synthetic melanocortin analogs (Melanotan I, II, PT-141, KPV) were derived and remains a cornerstone of melanocortin pharmacology research.
Research applications
What researchers are studying
NF-kB inhibition and cytokine reduction
BPC-157 has been shown across multiple models to reduce TNF-alpha, IL-1beta, and IL-6 levels in inflamed tissue. Its NF-kB inhibitory effect appears to be downstream of its interaction with the nitric oxide system, with studies showing it both reduces oxidative stress and normalizes eNOS activity in endothelial cells under inflammatory conditions.
Gut inflammation and mucosal protection
KPV administered orally or locally in colon models significantly reduces inflammatory markers and histological damage in animal models of inflammatory bowel disease. Given that KPV is a small tripeptide resistant to gastric degradation (the Pro-Val bond is unusually stable), it reaches intestinal tissue intact, making oral administration feasible — an important practical advantage over peptides requiring injection.
Analgesic pathway research
Ziconotide (Prialt) demonstrates that peptide-based analgesia through selective ion channel blockade is clinically viable. It blocks N-type voltage-gated calcium channels in dorsal horn neurons, preventing nociceptive signal transmission without the tolerance or dependency associated with opioid analgesics. This serves as proof of concept for the broader research interest in peptide-based pain management.
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