TNF-α , human

TNF-α (31-45), human acetate is a peptide of tumor necrosis factor-α.

TNF-α (31-45), human, is a peptide of tumor necrosis factor-α.

TNF-α (31-45), human (TFA), is a peptide of tumor necrosis factor-α (TNF alpha), an inflammatory cytokine that induces necrosis or apoptosis.

TNF-α (10-36), human (TFA) is a peptide of human TNF-α.

TNF-α (10-36), human, is a potent pro-inflammatory cytokine involved in the acute phase stress response.

Human TNF alpha (46-65) peptide.

TNF-α (31-45), human (TFA) is a peptide of tumor necrosis factor-α.

TNF-α (46-65), human (TFA) is a peptide of human TNF-α.

α-Melanocyte-stimulating hormone (α-MSH) is a 13-amino acid peptide hormone produced by post-translational processing of proopiomelanocortin (POMC) in the pituitary gland, as well as in keratinocytes, astrocytes, monocytes, and gastrointestinal cells.1It is an agonist of melanocortin receptor 3 (MC3R) and MC4R that induces cAMP production in Hepa cells expressing the human receptors (EC50s = 0.16 and 56 nM, respectively).2α-MSH (100 pM) reducesS. aureuscolony formation andC. albicansgerm tube formationin vitro.3It inhibits endotoxin-, ceramide-, TNF-α-, or okadaic acid-induced activation of NF-κB in U937 cells.1α-MSH reduces IL-6- or TNF-α-induced ear edema in mice.4It also prevents the development of adjuvant-induced arthritis in rats and increases survival in a mouse model of septic shock. Increased plasma levels of α-MSH are positively correlated with delayed disease progression and reduced death in patients with HIV.1 1.Catania, A., Airaghi, L., Colombo, G., et al.α-melanocyte-stimulating hormone in normal human physiology and disease statesTrends Endocrinol. Metab.11(8)304-308(2000) 2.Miwa, H., Gantz, I., Konda, Y., et al.Structural determinants of the melanocortin peptides required for activation of melanocortin-3 and melanocortin-4 receptorsJ. Pharmacol. Exp. Ther.273(1)367-372(1995) 3.Cutuli, M., Cristiani, S., Lipton, J.M., et al.Antimicrobial effects of a-MSH peptidesJ. Leukoc. Biol.67(2)233-239(2000) 4.Lipton, J.M., Ceriani, G., Macaluso, A., et al.Antiiinflammatory effect of the neuropeptide a-MSH in acute, chronic, and systemic inflammationAnn. N.Y. Acad. Sci.25(741)137-148(1994)

DSTYSLSSTLTLSK, a human peptide, facilitates the quantitative detection of Infliximab (Avakine), a chimeric monoclonal IgG1 antibody. Infliximab specifically targets and binds to TNF-α.

DSTYSLSSTLTLSK TFA, a generic human peptide, facilitates the quantitative detection of Infliximab (Avakine), a chimeric monoclonal IgG1 antibody targeting TNF-α, as indicated in study [1].

PMX-53, a macrocyclic complement 5a (C5a) peptidomimetic and C5a receptor antagonist (IC50 = 0.3 µM), effectively inhibits the C5a-induced secretion of myeloperoxidase (MPO) in isolated human polymorphonuclear leukocytes (PMNs). Administered orally at 10 mg kg, PMX-53 mitigates vascular leakage, PMN infiltration, and the production of TNF-α and IL-6 in a rat peritoneal Arthus reaction model. Additionally, in a 3-nitropropionic acid (3-NP)-induced Huntington's disease rat model, it alleviates body weight loss, anorexia, and striatal degeneration. Furthermore, at a dose of 3 mg kg, PMX-53 decreases atherosclerotic lesion size and lipid content in ApoE- - mice.

Cathelicidin-2 (CATH-2) (128-153) is a synthetic antimicrobial peptide derived from amino acids 128-153 of chicken CATH-2, demonstrating activity against pathogens such as E. coli, S. aureus, S. enteritidis, and B. globigii in a dose-dependent manner. At a concentration of 40 µM, it induces hemolysis in chicken erythrocytes without exhibiting cytotoxicity towards human peripheral blood mononuclear cells (PBMCs). Additionally, it stimulates the production of the chemokine CCL2 and suppresses LPS-induced secretion of TNF-α, IL-6, IL-8, and IL-10 in human PBMCs.

Pap12-6, an antibacterial peptide originating from the first twelve N-terminal amino acids of papiliocin found in P. xuthus larvae, exhibits activity against a range of eight Gram-negative bacteria (e.g., E. coli, P. aeruginosa, S. syphimurium with MIC50s=4-8 µM) and Gram-positive bacteria (e.g., S. aureus, methicillin-resistant S. aureus 3126, B. subtilis, and S. epidermidis with MIC50s=4-8 µM), without compromising the viability of human erythrocytes, mouse RAW 264.7 macrophages, human HaCaT keratinocytes, or human HEK293 kidney cells at 25 µM. It causes membrane depolarization in E. coli at 4 and 8 µM and, upon preincubation at 10 µM, decreases nitrite (NO2-), Tnf-α, and Il-6 secretion in LPS-stimulated RAW 264.7 macrophages. In a murine model, Pap12-6 enhances survival rates and diminishes colony forming units (CFUs) in several organs upon E. coli infection at 10 mg/kg and 1 mg/kg doses, respectively. Additionally, at a 1 mg/kg dose, it lowers serum aspartate aminotransferase (AST) and alanine transaminase (ALT) levels, as well as blood urea nitrogen levels in E. coli-induced sepsis, indicating its therapeutic potential for bacterial infections without affecting host cell viability.

Surfactant protein A (SP-A) (196-215) is a synthetic peptide derived from the C-terminal carbohydrate recognition domain of human SP-A, specifically amino acids 196-215. This peptide suppresses LPS-induced TNF-α release in JAWSII mouse dendritic cells at 1 and 10 µM concentrations and promotes phagocytosis of P. aeruginosa at a 75 µM concentration. Furthermore, intratracheal administration of SP-A (196-215) at a dose of 50 µg per animal reduces disease severity and lung colony-forming units in mice infected with P. aeruginosa.

Toll-like receptor 2/6 (TLR2/6) agonist. Induces TNF-α production in human mononuclear cells. Also induces proliferation and activation of mouse splenic B cells.