ACT-660602 is an orally active antagonist of chemokine receptor (CXCR3) with an IC50 value of 204 nM. ACT-660602 inhibits T-cell migration and shows efficacy in acute lung ingury model. ACT-660602 can be used for autoimmune diseases research[1][2].
CXCR2 antagonist 3 (compound 11h) is a potent antagonist of CXC chemokine receptor 2 (CXCR2). CXCR2 antagonist 3 demonstrates double-digit nanomolar potencies against CXCR2 and significantly inhibited neutrophil infiltration into the air pouch. CXCR2 antagonist 3 reduces the infiltration of neutrophils and MDSCs and enhance the infiltration of CD3+ T lymphocytes into the Pan02 tumor tissues[1].
CXCR4 antagonist 8 (Compound 3) is a CXCR4 antagonist with an IC50 of 57 nM. CXCR4 antagonist 8 inhibits CXCL12 induced cytosolic calcium increase with an IC50 of 0.24 nM. CXCR4 antagonist 8 inhibits CXLC12/CXCR4 mediated cell migration[1].
Ac-Pro-Gly-Pro-OH is an endogenous degradation product of extracellular collagen and can be used as CXCR2 agonist. Ac-Pro-Gly-Pro-OH elicits bactericidal activity and inhibits lung inflammation, reducing immune cell apoptosis. Ac-Pro-Gly-Pro-OH enhances the production of type 1 cytokines (IFN-γ and IL-12) but inhibits the production of proinflammatory cytokines. Ac-Pro-Gly-Pro-OH has the potential for the research of sepsis[1][2].
ACT-1004-1239 is a potent, selective, orally available CXCR7 antagonist with an IC50 value of 3.2 nM.
AZD8797 is an allosteric non-competitive modulator of the human CX3CR1 receptor; antagonizes CX3CR1 and CXCR2 with Kis of 3.9 and 2800 nM, respectively.
CXCR7 modulator 1 (compound 25) is a potent and orally bioavailable peptoid hybrid CXCR7 modulator, with a Ki of 9 nM[1].
BKT140 4-fluorobenzoyl is a novel CXCR4 antagonist with an IC50 vakue of ～1 nM. Sequence: 4F-Benzoyl-Arg-Arg-{2-Naph-Ala}-Cys-Tyr-{Cit}-Lys-Lys-Pro-Tyr-Arg-{Cit}-Cys-Arg-NH2(Disulfide bridge: Cys4-Cys13).
AZD4721 (RIST4721) is the potent and orally active antagonist of acidic CXC chemokine receptor 2 (CXCR2). AZD4721 has the potential for the research of inflammatory disease[1].
CXCR4-IN-1 (Example C5) is a CXCR4 inhibitor (IC50: 20 nM). CXCR4-IN-1 can be used for research of cancer, HIV, diabetic retinopathy, inflammation, etc[1].
CTCE-0214 is a chemokine CXC receptor 4 (CXCR4) agonist, SDF-1α (stromal cell-derived factor-1α) peptide analog. CTCE-0214 shows anti-inflammatory activity, and can be used in inflammation sepsis and systemic inflammatory syndromes research[1][2][3].
ACT-777991 is an orally active and selective CXCR3 antagonist. ACT-777991 has microsomes and hepatocytes stability across animal models. ACT-777991 inhibits the migration of activated T cells toward CXCL11[1].
NUCC-390 is a novel and selective small-molecule CXCR4 receptor agonist. NUCC-390 can induce internalization of CXCR4 receptors[1].
PS372424 hydrochloride, a three amino-acid fragment of CXCL10, is a specific human CXCR3 agonist with anti-inflammatory activity. PS372424 hydrochloride prevents human T-cell migration in a humanized model of arthritic inflammation[1][2].
Reparixin L-lysine salt is an allosteric inhibitor of chemokine receptor 1/2 (CXCR1/2) activation.
CXCR4 antagonist 1 is a potent CXCR4 antagonist. CXCR4 antagonist 1 has anti-HIV activity[1].
SX-682 is an orally bioavailable, potent allosteric inhibitor of CXCR1 and CXCR2. SX-682 can block tumor myeloid-derived suppressor cells (MDSCs) recruitment and enhance T cell activation and antitumor immunity[1].
KRH-3955 hydrochloride is an orally bioavailable CXCR4 antagonist. KRH-3955 hydrochloride inhibits SDF-1α binding to CXCR4 with an IC50 of 0.61 nM. KRH-3955 hydrochloride is also a highly potent and selective inhibitor of X4 HIV-1, with an EC50 of 0.3 to 1.0 nM[1].
VUF11211 is an effective antagonist of CXCR3 that acts by extending from the minor pocket into the major pocket of the transmembrane domains.
LIT-927 is a locally and orally active CXCL12 neutraligand with anti-inflammatory effect, with a Ki of 267 nM for CXCL12-TR binding.
HF50731 (HF-50731) is a novel potent, selective CXCR4 antagonist with Ki of 19.8 nM in the CXCR4 competitive binding assay.HF50731 significantly inhibited SDF-1α-induced calcium mobilization (IC50=621 nM) and cell migration, and blocked HIV-1 infection via antagonizing CXCR4 coreceptor function (IC50=1.5 uM).The structure-activity relationship analysis demonstrated that HF50731 could primarily occupy the minor subpocket of CXCR4 and partially bind in the major subpocket by interacting with residues W94, D97, D171, and E288.
Burixafor hydrobromide (TG-0054 hydrobromide) is an orally bioavailable and potent antagonist of CXCR4 and a well water soluble anti-angiogenic drug that is of potential value in treating choroid neovascularization[1]. Burixafor hydrobromide (TG-0054 hydrobromide) mobilizes mesenchymal stem cells, attenuates inflammation, and preserves cardiac systolic function in a porcine model of myocardial infarction[2].
PS372424, a three amino-acid fragment of CXCL10, is a specific human CXCR3 agonist with anti-inflammatory activity, which inhibits the binding of CXCR3 ligand CXCL10 to CXCR3 receptor with IC50 of 42 nM[1][2][3].
Olaptesed pegol (NOX-A12) L-oligoribonucleotide aptamer targeting CXCL12 based on a pegylated structure. Olaptesed pegol neutralizes CXCL12, and CXCL12 inhibition mobilizes chronic lymphocytic leukemia cells into the circulation and prevents their homing into the protective microenvironment[1].
Zaprinast (M&B 22948) is an inhibitor of cGMP-selective Phosphodiesterases(PDEs)[1]. Zaprinast is a G protein-coupled receptor (GPR) 35 agonist which activates rat GPR35 strongly and activates human GPR35 moderately[2]. Zaprinast reduces vessel remodeling through antiproliferative and proapoptotic effects[3].
AZ10397767 is a potent, selective CXCR2 inhibitor that inhibits CXCL8 binding to CXCR2 with pIC50 of 9.0; weakly inhibits CXCL8 binding to CXCR1 with pIC50<7, and no affinity for CCR2 and CCR5; significantly attenuates IL-8-induced c-FLIP mRNA up-regulation whereas inhibition of AR- and/or NF-kappaB-mediated transcription attenuated IL-8-induced c-FLIP expression in LNCaP and PC3 cells, respectively; attenuates oxaliplatin-induced NF-kappaB activation, increases oxaliplatin cytotoxicity, and potentiates oxaliplatin-induced apoptosis in AIPC cells.