formyl peptide receptor

FPR A14 is an agonist of formyl peptide receptor (FPR) and induces cell differentiation.

N-Formyl-Nle-Leu-Phe-Nle-Tyr-Lys TFA (For-Nle-Leu-Phe-Nle-Tyr-Lys-OH (TFA)) (For-Nle-Leu-Phe-Nle-Tyr-Lys-OH TFA) is a formyl peptide receptor (FPR) agonist and a potent chemoattractant for human neutrophils, with its radioiodinated form retaining full biological activity.

Ac9-25 acetate is an annexin AI peptide and activates the neutrophil reduced nicotinamide adenine dinucleotide phosphate oxidase through FPR but not through FPRL1.

ACT-389949 is a potent and selective agonist of formyl peptide receptor type 2 (FPR2)/Lipoxin A4 receptor (ALX), with an EC50 of 3 nM for FPR2/ALX internalization into monocytes. It has the potential for the treatment of inflammatory disorders.

Boc-MLF (TFA) is a specific antagonist of formyl peptide receptor (FPR) and also inhibits signaling through FPRL1 at higher concentrations.

FPR Agonist 43 is a dual agonist of formyl peptide receptor 1 and formyl peptide receptor 2 (FPR2)/ALX.

Rezuforimod is an agonist of the N-formyl peptide receptor like-1 receptor (FPRL-1), with an EC50 of 0.88 nM in CHO-Ga16 cells. It exhibits anti-inflammatory properties.

LL-37 is a cationic and α-helical antimicrobial peptide expressed in human bone marrow, testis, granulocytes, and gingival epithelium and is upregulated in psoriatic lesions. It inhibits growth of Gram-positive E. coli D21 and Gram-negative B. megatarium in a concentration-dependent manner and LL-37 expression is induced in A549 epithelial cells, alveolar macrophages, neutrophils, and monocyte-derived macrophages following M. tuberculosis infection. LL-37 binds sheep erythrocytes coated with S. minnesota Re-LPS and induces agglutination with a minimal agglutinating concentration (MAC) of 12.1 μg/ml. It is a chemoattractant for, and can induce calcium mobilization in, human monocytes, neutrophils, and T cells that naturally express formyl peptide receptor-like 1 (FPRL1) and FPRL1-transfected HEK293 cells. LL-37 (10-15 μM) pretreatment of dengue virus type 2 (DENV-2) reduces its infectivity as well as levels of viral genomic RNA and NS1 antigen. In vivo, LL-37 inhibits cecal ligation and puncture-induced caspase-1 activation and pyroptosis of peritoneal macrophages, reduces levels of the inflammatory cytokines IL-1β, IL-6, and TNF-α, and improves survival in polybacterial septic mice.

BMS-986235 (LAR-1219) is a selective and orally active agonist of formyl peptide receptor 2 (FPR2) with EC50s of 0.41 nM for hFPR2 and 3.4 nM for mFPR2. BMS-986235 can be used in studies on the prevention of heart failure.

AG-09/1 is a selective and potent formyl peptide receptor 1 (FPR1) agonist that activates chemotaxis in human neutrophils.

{Boc}-Phe-Leu-Phe-Leu-Phe ({Boc}-FLFLF) is a selective antagonist of the formyl peptide receptor (FPR) family, effectively inhibiting receptor activity in response to formyl peptides.

Boc-MLF (TFA), a peptide antagonist specific to the formyl peptide receptor (FPR), also inhibits signaling through formyl peptide receptor like 1 (FPRL1) at elevated concentrations [1].

WKYMVM is a N-formyl peptide receptor (FPR1) agonist.

WKYMVM 2TFA is a N-formyl peptide receptor (FPR1) agonist.

PBP10, a cell-permeable and selective gelsolin-derived peptide, inhibits formyl peptide receptor 2 (FPR2) over FPR1 [1]. This 10-amino acid (AA) peptide features a rhodamine conjugation at its N terminus, exhibiting bactericidal activity against both gram-positive and gram-negative bacteria while mitigating microbial-induced inflammatory effects [2].

MMK1 TFA is a potent, selective agonist for the human formyl peptide receptor like-1 (FPRL-1/FPR2), exhibiting EC50 values of <2 nM for FPRL-1 and >10,000 nM for FPR1. This compound acts as a powerful chemotactic and calcium-mobilizing agent, effectively activating phagocytic leukocytes. It significantly enhances the Pertussis Toxin-sensitive production of proinflammatory cytokines IL-1b and IL-6 by human monocytes. Additionally, MMK1 TFA has been demonstrated to exhibit anxiolytic-like activity [1] [2] [3] [4].

Ac9-25 TFA, an N-terminal peptide of Annexin I, functions as a formyl peptide receptor (FPR) agonist, activating neutrophil NADPH oxidase via FPR [1] [2].

WKYMVM-NH2 TFA, a potent agonist for N-formyl peptide receptor (FPR1) and FPRL1/2, activates key leukocyte effector functions including chemotaxis, complement receptor-3 mobilization, and NADPH oxidase activation, as documented in references [1] [2] [3].

{Boc}-Phe-Leu-Phe-Leu-Phe TFA is a selective antagonist of the formyl peptide receptor (FPR) family, effectively inhibiting FPR-mediated actions [1].

Compound 24a, an FPR1 antagonist, demonstrates potent inhibition of the formyl peptide receptor 1 (FPR1) with an IC50 value of 25 nM. It impedes cell proliferation and promotes apoptosis, thereby inhibiting cell growth. This compound also attenuates cell migration and concurrently promotes angiogenesis [1].

Compound 25b, an FPR1 antagonist, exhibits potent inhibition of the formyl peptide receptor 1 with an IC50 of 70 nM. It concurrently hampers cell proliferation and triggers apoptosis, diminishing cell growth and migration, yet paradoxically augments angiogenesis [1].

HCH6-1 is a competitive Formyl peptide receptor 1 (FPR1) antagonist.

N-Boc-Phe-Leu-Phe-Leu-Phe (Boc-FLFLF) is a formyl peptide receptor 1 (FPR1) antagonist that increases pain effects and inhibits the antinociceptive activity of annexin. Boc-FLFLF is extensively used in FPR research.

N-Formyl-Met-Ala-Ser is a peptide that binds to formyl peptide receptors on neutrophils. N-Formylmethionine-containing peptides, including the most potent and well-known member N-formyl-Met-Leu-Phe [FMLP or fMet-Leu-Phe], stimulate human neutrophils through a receptor-dependent mechanism.