α5β1 Inhibitor

Cilengitide (EMD 121974) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC₅₀ values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors.

RGD peptide (GRGDNP) is an inhibitor of integrin-ligand interactions. RGD peptide (GRGDNP) competitively inhibits α5β1 binding with extracellular matrice (ECM). RGD peptide (GRGDNP) promotes apoptosis through activation of conformation changes that enhance pro-caspase-3 activation and autoprocessing. RGD peptide (GRGDNP) plays an important role in cell adhesion, migration, growth, and differentiation.

Cilengitide TFA (EMD 121974 TFA) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC₅₀ values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide TFA inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide TFA inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide TFA can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors.

Volociximab (M200) is a chimeric human/murine IgG4 antibody IIA1 targeting integrin α5β1 (EC₅₀=0.2 nM). Integrin α5β1 is a major fibronectin receptor involved in angiogenesis. Volociximab has antiangiogenic and antitumor activities and inhibits the proliferation of human umbilical vein vascular endothelial cells (HUVECs).

RGD peptide (GRGDNP) TFA is an inhibitor of integrin-ligand interactions. RGD peptide (GRGDNP) TFA competitively inhibits α5β1 binding with extracellular matrice (ECM). RGD peptide (GRGDNP) TFA promotes apoptosis through activation of conformation changes that enhance pro-caspase-3 activation and autoprocessing. RGD peptide (GRGDNP) TFA plays an important role in cell adhesion, migration, growth, and differentiation.

α5β1 integrin-IN-1 is a potent and selective α5β1 integrin inhibitor with an IC₅₀ value of approximately 0.4 nM (pIC₅₀ = 9.4 M). α5β1 integrin-IN-1 disrupts the interaction between α5β1 integrin and fibronectin, thereby blocking smooth muscle tension transmission and α5β1 integrin-mediated cell adhesion. α5β1 integrin-IN-1 can be used in the research of asthma and allergic asthma.

Anti-Integrin α5β1 Antibody is an anti-human monoclonal antibody targeting integrin α5β1.

MINT1526A (RG-7594) is a humanized IgG1 monoclonal antibody inhibitor targeting α5β1 integrin. MINT1526A has significant anti-angiogenic activity. MINT1526A can be used for cancers research.

IPS-05002 is an α5β1 antagonist. IPS-05002 can inhibit VEGF-stimulated human umbilical vein endothelial cell (HUVEC) proliferation, adhesion, and migration, and also suppresses tubular network formation. IPS-05002 can upregulate IKB-β, XRCC4, and downregulate Cdc6 in VEGF-induced HUVECs. IPS-05002 can be used for the study of tumor angiogenesis.

CLT-28643 is an integrin α5β1 inhibitor. CLT-28643 can inhibit the high expression of integrin α5β1 in the bleb at early time-points after surgery and promote wound healing process.

Cilengitide hydrochloride (EMD 121974 hydrochloride) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC₅₀ values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide hydrochloride inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide hydrochloride inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide hydrochloride can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors.