antiintegrins

Anti-integrins are a class of therapeutic or research agents that inhibit integrins, a family of transmembrane receptors that mediate cell adhesion by binding extracellular matrix proteins and counter-receptors such as ICAMs and VCAMs. Inhibitors can be monoclonal antibodies, antibody fragments, small molecules, or peptide mimetics that block ligand binding, disrupt integrin activation, or interfere with inside-out signaling, thereby reducing cell adhesion, migration, and signaling relevant to inflammation, thrombosis, angiogenesis, and tumor progression.

Mechanistically, anti-integrins may act as competitive antagonists of the ligand-binding site, allosteric modulators that alter receptor conformation, or agents that hinder receptor clustering and activation. Therapeutic goals include preventing platelet aggregation, reducing leukocyte trafficking to inflamed tissues, and inhibiting integrin-driven angiogenesis and metastasis. The specificity of inhibition often targets particular integrin heterodimers such as GPIIb/IIIa (αIIbβ3) in platelets or α4β7 and α4β1 in immune cells, as well as αv-containing integrins involved in angiogenesis.

Clinical use spans several areas. In cardiovascular disease, glycoprotein IIb/IIIa inhibitors like abciximab, eptifibatide, and tirofiban limit thrombosis during coronary interventions. In autoimmune and inflammatory disorders, antibodies against α4 integrins (natalizumab) and α4β7 (vedolizumab) block leukocyte trafficking and are approved for multiple sclerosis and inflammatory bowel disease, with vedolizumab offering gut-selective activity. Anti-integrins have been explored in cancer and fibrosis (e.g., inhibitors of αvβ3/β5), though broader clinical success has been variable, and safety concerns—such as infection risk and rare cases of progressive multifocal leukoencephalopathy—have shaped development.

Research use includes dissection of integrin function in cell adhesion and migration, as well as preclinical evaluation of integrin-targeted therapies.