BNTA is a potent extracellular matrix (ECM) modulator. In a rat model of arthritis, BNTA modulates arthritis by promoting the synthesis of cartilage structural molecules on chondrocytes through the induction of superoxide dismutase 3 (SOD3) and regulating chondrogenesis through superoxide anion elimination.

BNTA (0.01-10 μM; 1-7 days) exhibits no reduction in cell viability for human osteoarthritis chondrocytes and primary chondrocytes isolated from rats.[1]
BNTA (0.1 μM; 2 days) induces a significant elevation in SOX9 protein expression. Notably, BNTA markedly enhances the protein levels of COL2A1 and SOX9 in rat osteoarthritis (OA) chondrocytes induced by IL1β.[1]
BNTA (0.01-10 μM; 6 hours) enhances the expression levels of extracellular matrix (ECM)-related genes, including COL2A1, ACAN, proteoglycan 4 (PRG4), and SRY-box 9 (SOX9) in human osteoarthritis (OA) chondrocytes. In IL1β-induced rat OA chondrocytes, BNTA elevates Col2a1, Acan, Prg4, and Sox9 mRNA levels, with the most significant effects observed around 0.1 μM.[1]
BNTA (10 μM; 5 days) increases proteoglycan staining in ATDC5 cells.[1]
BNTA (0.01-1 μM; 2 or 3 weeks) enhances anabolism and inhibits inflammatory response in osteoarthritis cartilage explants.[1]

BNTA (0.015-1.5 mg/kg; intra-articular injection; twice a week for 4 and 8 weeks; Male SD rats ) attenuated post-traumatic osteoarthritis development after intra-articular injection well tolerated and could attenuate OA progression developed after anterior cruciate ligament transection (ACLT) in rats.[1]