Integrin alpha-V beta-1, Integrin alpha-V beta-3, and Integrin alpha-V beta-6 receptor (Integrin αvβ1, αvβ3, and αvβ6)

Integrin alpha-V beta-1 (αvβ1), alpha-V beta-3 (αvβ3), and alpha-V beta-6 (αvβ6) are members of the integrin family of heterodimeric transmembrane receptors, each comprising a shared alpha-V (ITGAV) subunit paired with a distinct beta subunit (ITGB1, ITGB3, ITGB6, respectively)[2][3][6]. These receptors mediate cell-cell and cell-extracellular matrix adhesion by recognizing specific amino acid motifs (notably RGD sequences) in ECM proteins such as fibronectin, vitronectin, tenascin, osteopontin, and TGF-β latency-associated peptides[1][3]. Integrins not only anchor cells but also transduce bidirectional signals, regulating cellular processes including migration, proliferation, survival, angiogenesis, and immune response[2][3][5]. αvγ is well known for its role in angiogenesis, tumor growth, and metastasis, making it a longstanding therapeutic target in oncology[1][3]. αvζ is upregulated in several epithelial cancers and fibrotic diseases and is a key activator of TGF-β, contributing to tissue fibrosis and tumor progression[1][7]. αvα, more recently recognized, is involved in TGF-β activation and fibrosis and is emerging as a novel therapeutic target[1]. Multiple therapeutic agents—including antibodies, peptides, and small molecules—have been developed to selectively block these integrins, aiming to inhibit tumor angiogenesis, cancer cell migration, and fibrotic processes[1][3]. Due to their widespread physiological expression and role in normal tissue maintenance, safety concerns include bleeding, delayed wound healing, and immunomodulation[3]. Integrin ligands and receptor expression serve as biomarkers for diagnosis, prognostic stratification, and patient selection in clinical trials.

Other names

Vitronectin receptor (for αvβ3 and αvβ5)αvβ class integrinsITGAV/ITGB1 (αvβ1), ITGAV/ITGB3 (αvβ3), ITGAV/ITGB6 (αvβ6)CD51/CD29 (αvβ1), CD51/CD61 (αvβ3), CD51/CD66 (less common for αvβ6)

Antagonism of ligand binding (prevents attachment to ECM proteins such as fibronectin, vitronectin, osteopontin); Inhibition of TGF-β activation (especially αvβ6 and αvβ1); Blockade of angiogenesis and tumor cell migration