αvβ5 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.

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.

αvβ5 integrin-IN-1 (Compound 12) is a selective αvβ5 inhibitor (pIC₅₀ = 8.2). αvβ5 integrin-IN-1 exhibits 800-fold selectivity for αvβ5 versus αvβ3.

PAS-003 is a humanized monoclonal antibody targerting α5β1 integrin. PAS-003 modulates immune cell migration, immune cell adhesion, improves behavior, and improves survival in ALS mouse models. PAS-003 can be used for the research of amyotrophic lateral sclerosis.

αvβ5 integrin-IN-3 is an orally active, selective αVβ5 integrin inhibitor with an IC₅₀ value of 0.61 nM. αvβ5 integrin-IN-3 inhibits αVβ1, αVβ3 and αVβ6 integrins with IC₅₀ values of 21 nM, 5.5 nM and 18 nM, respectively. αvβ5 integrin-IN-3 reduces total Collagen content in a mouse unilateral ureteral obstruction model. αvβ5 integrin-IN-3 can be used for the research of renal fibrosis.

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.