formyl peptide receptor

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

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.

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].

WRW4 TFA is a formyl peptide receptor-like 1 (FPRL1) antagonist that specifically prevents the binding of WKYMVm to FPRL1 with an inhibition concentration (IC50) of 0.23 μM. It uniquely blocks the rise in intracellular calcium triggered by FPRL1 agonists such as MMK-1, amyloid beta42 (Abeta42) peptide, and F peptide [1].

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-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.

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.