Inflammation Peptides

An endogenous cardiovascular peptide that signals through the APJ receptor, studied for heart failure, cardiac repair, and cardioprotection with multiple synthetic analogs in clinical development.

A non-erythropoietic EPO analog studied for nerve repair and neuropathic pain conditions.

A pentadecapeptide derived from human gastric juice, studied for tissue repair and gut-protective properties.

A combined formulation of BPC-157 and TB-500, the two most commonly paired tissue repair peptides.

A synthetic 15-amino-acid peptide derived from the IL-10 receptor alpha chain, granted FDA breakthrough therapy status for systemic lupus erythematosus (SLE) after Phase III trial success.

A brain-targeting tetrapeptide studied for neuroprotection and targeted drug delivery to injured brain and spinal cord tissue.

A long-acting, once-weekly dual GLP-1 and GLP-2 receptor agonist peptide (Zealand Pharma) developed for obesity, uniquely pairing GLP-1-driven weight loss with GLP-2 activation intended to improve intestinal barrier function and reduce obesity-related low-grade inflammation; development was paused in November 2025.

Difelikefalin (Korsuva in the U.S., Kapruvia in Europe) is a synthetic tetrapeptide built entirely from D-amino acids - D-Phe-D-Phe-D-Leu-D-Lys capped with a 4-aminopiperidine-4-carboxylic acid - that acts as a selective agonist at the kappa opioid receptor. Its defining property is what it cannot do: the molecule is hydrophilic and bulky enough that it does not meaningfully cross the blood-brain barrier, so it reaches kappa receptors on peripheral sensory nerve endings, keratinocytes and immune cells while leaving the central kappa receptors that produce dysphoria and hallucinations largely untouched. It has no activity at the mu opioid receptor, so it carries neither euphoria nor respiratory depression. In the Phase 3 KALM-1 and KALM-2 trials in hemodialysis patients with moderate-to-severe chronic-kidney-disease-associated pruritus, roughly 40-51% of difelikefalin-treated patients achieved a clinically meaningful (>=3-point) reduction on the 10-point Worst Itching Intensity NRS at 12 weeks versus roughly 20-28% on placebo. The FDA approved intravenous difelikefalin in August 2021; the EU approved it as Kapruvia in April 2022.

A first-in-class, intravenous immunomodulatory fusion peptide derived from histidyl-tRNA synthetase that selectively binds neuropilin-2 (NRP2) to dampen inflammation in the lung; in Phase 3 development for pulmonary sarcoidosis, an interstitial lung disease.

A naturally occurring copper-binding peptide studied for skin regeneration, wound healing, and anti-aging effects.

The first FDA-approved targeted oral macrocyclic peptide — an IL-23 receptor antagonist for moderate-to-severe plaque psoriasis, marking a new era for oral peptide therapeutics.

A multi-peptide blend combining BPC-157, TB-500, GHK-Cu, and KPV for comprehensive tissue repair and anti-inflammatory support.

A tripeptide derived from alpha-MSH, studied for anti-inflammatory and gut-protective properties.

A synthetic peptide tight junction regulator in clinical trials for celiac disease, designed to prevent intestinal permeability caused by gluten exposure.

A human antimicrobial peptide studied for innate immunity, wound healing, and biofilm disruption.

A PEGylated cyclic-peptide inhibitor of complement component 3 (C3) built from two compstatin (Cp05) peptide domains bridged by a 40-kDa PEG chain; marketed as Empaveli/Aspaveli (subcutaneous, for paroxysmal nocturnal hemoglobinuria and, since July 2025, C3 glomerulopathy and primary IC-MPGN) and Syfovre (intravitreal, for geographic atrophy in age-related macular degeneration). It is one of the few complement-targeting therapeutic peptides to reach the market.

A semi-synthetic polysaccharide FDA-approved for interstitial cystitis and studied for joint health applications.

A naturally occurring peptide involved in cell migration and tissue repair, studied for wound healing and recovery.

A thymic peptide approved in some countries for immune modulation, studied for viral infections and cancer adjunct therapy.

A neuropeptide with broad neuroimmune functions, studied for inflammatory conditions and nerve repair.

An investigational, once-weekly injectable long-acting analogue of the human hormone relaxin-2 from Eli Lilly, engineered as a selective agonist of the relaxin family peptide receptor 1 (RXFP1) and studied for chronic kidney disease and heart failure. Natural relaxin is a peptide hormone with vasodilatory, anti-inflammatory and anti-fibrotic effects, but it clears from the body within hours; volenrelaxin fuses relaxin-2 to an albumin-binding VHH (single-domain antibody) fragment that latches onto serum albumin to extend its half-life beyond ~40 hours in animals, allowing once-weekly subcutaneous dosing. In a randomized Phase 1 trial it increased effective renal plasma flow (a marker of kidney perfusion) by roughly 44-50% versus placebo, supporting development in chronic kidney disease and heart failure. However, in the Phase 2 RELAXIN-LA trial (n=332) in people with worsening heart failure with preserved ejection fraction (HFpEF), the program hit a wall: although the lowest 25 mg dose modestly improved the primary imaging endpoint (left atrial reservoir strain), the pooled higher doses were associated with WORSENING congestion - rising NT-proBNP, more estimated plasma volume, and a numerically higher rate of heart-failure hospitalizations - prompting the sponsor to stop the trial early, and the authors concluded the data do NOT support further evaluation of volenrelaxin in worsening HFpEF. Volenrelaxin is an investigational prescription-stage medicine studied only in clinical trials - it is not approved anywhere and is not a supplement or research chemical.

An investigational, fully human monoclonal antibody that neutralizes the pro-inflammatory cytokine interleukin-6 (IL-6) to test whether lowering vascular inflammation - independently of cholesterol - can prevent heart attacks, strokes and cardiovascular death. Given as a low-volume, once-monthly 15 mg subcutaneous injection (half-life ~57 days), ziltivekimab was originally developed by Corvidia Therapeutics and acquired by Novo Nordisk in 2020 for up to $2.1 billion. It is the flagship clinical test of the 'residual inflammatory risk' hypothesis that grew out of the CANTOS trial of the IL-1 beta antibody canakinumab: the idea that many high-risk patients keep having cardiovascular events because of ongoing inflammation (marked by high-sensitivity C-reactive protein, hsCRP) even when LDL cholesterol is well controlled. In the Phase 2 RESCUE trial ziltivekimab cut hsCRP by up to ~92%, and it advanced into three large Phase 3 cardiovascular outcomes trials - ZEUS, HERMES and ARTEMIS. On July 31, 2026, Novo Nordisk announced that the pivotal ZEUS trial (>6,300 patients with atherosclerotic cardiovascular disease, chronic kidney disease and inflammation) MISSED its primary endpoint: despite clear target engagement (large falls in free IL-6 and hsCRP), ziltivekimab did not reduce major adverse cardiovascular events versus placebo (hazard ratio 0.99, 95% CI 0.88-1.11). The heart-failure trial HERMES and the post-heart-attack trial ARTEMIS continue, with readouts expected in the first half of 2027. Ziltivekimab is a prescription-stage investigational biologic - it is not approved anywhere and is not a supplement or research chemical.

Barzolvolimab (development code CDX-0159) is an investigational humanized IgG1 monoclonal antibody from Celldex Therapeutics that works by a mechanism new to allergy and dermatology: it depletes mast cells. It binds with high specificity to the KIT receptor (CD117), a receptor tyrosine kinase that mast cells depend on for their growth, survival and activation, and blocks KIT from being switched on by its natural ligand, stem cell factor (SCF). Because mast cells cannot survive without KIT signaling, blocking the receptor lowers mast-cell numbers throughout the body - an effect visible as a dose-dependent fall in blood tryptase (a mast-cell marker) and a drop in mast cells in the skin. Mast cells are the central drivers of chronic urticaria (chronic hives): when they release histamine and other mediators they cause the wheals, angioedema and itch that define the disease, so removing the cells themselves is a more upstream approach than blocking a single downstream signal. Barzolvolimab's lead program is chronic spontaneous urticaria (CSU) that no longer responds to antihistamines, where it is being tested in two large replicate Phase 3 trials, EMBARQ-CSU1 and EMBARQ-CSU2, which together enrolled 1,939 patients - the largest Phase 3 program ever run in antihistamine-refractory CSU - with topline results expected in late 2026 and a planned regulatory (BLA) filing in 2027. It has also shown strong Phase 2 results in the chronic inducible urticarias - cold urticaria and symptomatic dermographism - and is being explored in prurigo nodularis, atopic dermatitis and eosinophilic esophagitis. Barzolvolimab is an investigational biologic given by subcutaneous injection under clinical-trial or specialist supervision; it is not approved, and it is not a supplement, nootropic or research chemical.

Amlitelimab (SAR445229, formerly KY1005) is a fully human, non-T-cell-depleting monoclonal antibody from Sanofi that blocks OX40 ligand (OX40L), a costimulatory signal that drives and sustains T-cell-mediated inflammation. Rather than neutralizing a single cytokine like IL-4/IL-13 (dupilumab) or IL-5 (depemokimab), amlitelimab acts upstream at the OX40-OX40L checkpoint to dampen a broad, memory-driven inflammatory program without depleting T cells. Its lead (anchor) indication is moderate-to-severe atopic dermatitis in people aged 12 and older, where a distinctive feature is very infrequent dosing: after a loading dose it is given subcutaneously as little as four times a year (every 12 weeks). In the Phase 3 program - COAST 1, COAST 2 and SHORE - amlitelimab met its primary endpoints with EASI-75 and vIGA-AD 0/1 responses that increased over time, though COAST 2's absolute response rates were more modest and some observers called that readout mixed. Amlitelimab is investigational and not yet approved by any regulator; Sanofi originally gained it through its ~$1.1B acquisition of Kymab in 2021.

Frexalimab (SAR441344) is an investigational second-generation, fully human monoclonal antibody from Sanofi that blocks CD40 ligand (CD40L, also called CD154), a costimulatory 'second signal' that helps activate B cells, T cells and antigen-presenting cells and drives adaptive autoimmunity. Rather than depleting immune cells, frexalimab interrupts the CD40-CD40L checkpoint upstream - a mechanism related to but distinct from the OX40-OX40L blockade of amlitelimab. Its lead indication is relapsing multiple sclerosis (RMS), with a second program in nonrelapsing secondary progressive MS (nrSPMS). In the Phase 2 relapsing-MS trial (NCT04879628, published in the New England Journal of Medicine in 2024), frexalimab cut the number of new gadolinium-enhancing brain lesions at week 12 by 89% (higher-dose IV arm) and 79% (lower-dose subcutaneous arm) versus placebo, and open-label extensions out to two and three years show that disease control and reductions in neurofilament light have been sustained. Crucially, frexalimab is engineered so its Fc region does not activate platelets, which is designed to avoid the thromboembolic complications that halted first-generation anti-CD40L antibodies decades ago. It is now in the Phase 3 FREXALT (relapsing MS, versus teriflunomide) and FREVIVA (nrSPMS, versus placebo) trials, with additional Phase 2 programs in type 1 diabetes (FABULINUS) and systemic lupus erythematosus; a Sjogren's syndrome study was discontinued in 2024 after it fell short on efficacy. Frexalimab is investigational and not approved by any regulator.

Rocatinlimab (AMG 451 / KHK4083) is an investigational anti-OX40 monoclonal antibody developed by Kyowa Kirin and Amgen for moderate-to-severe atopic dermatitis (eczema). Unlike amlitelimab, which blocks the OX40 ligand (OX40L) on antigen-presenting cells without depleting cells, rocatinlimab binds the OX40 receptor directly on activated pathogenic T cells and reduces (depletes) them - a 'T-cell rebalancing' approach meant to reset the immune drivers of chronic inflammation rather than continuously neutralize a single cytokine. In the large Phase 3 ROCKET program the drug met its co-primary endpoints: in ROCKET-IGNITE (NCT05398445; 769 adults, added to topical therapy) week-24 EASI-75 reached about 42% (higher dose) and 36% (lower dose) versus roughly 13% on placebo, and vIGA-AD 0/1 reached about 24% and 19%; in the ROCKET-HORIZON monotherapy study (NCT05651711) EASI-75 was about 33% versus 14% on placebo, though the drug showed no superiority over dupilumab. The pooled Phase 3 results were published in The Lancet in 2025. Despite hitting its endpoints, the program then unraveled on two fronts: in January 2026 Amgen ended the collaboration on strategic-portfolio grounds and returned global rights to Kyowa Kirin, and on March 3, 2026 Kyowa Kirin discontinued ALL rocatinlimab clinical trials - across atopic dermatitis, prurigo nodularis and uncontrolled asthma - after a safety review identified cases of Kaposi's sarcoma (one newly confirmed and one suspected, in addition to a previously confirmed case) that suggested a possible mechanistic link to OX40-pathway modulation. Rocatinlimab is investigational, was never approved by any regulator, and its clinical development has been halted.