|BNTA Catalog No.GC60650|
Sample solution is provided at 25 µL, 10mM.
GlpBio Products Cited In Reputable Papers
|Cas No.||685119-25-9||SDF||Download SDF|
|Solubility||N/A||Storage||Store at -20°C|
|General tips||For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.|
|Shipping Condition||Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
BNTA, a potent extracellular matrix (ECM) modulator, facilitates cartilage structural molecule synthesis on chondrocytes by activating superoxide dismutase 3 (SOD3). BNTA promotes cartilage extracellular matrix generation and inhibits osteoarthritis development. BNTA has the potential for the research of osteoarthritis.
BNTA (0.01-10 μM; 1-7 d) does not decrease cell viability of human osteoarthritis chondrocytes and rat primary chondrocytes.BNTA (0.1 μM; 2 d) increases SOX9 protein markedly.BNTA (0.1 μM; 2 d) remarkably increases the COL2A1 and SOX9 protein levels in IL1β-induced rat OA chondrocytes.BNTA (10 μM; 5 d) increases proteoglycan staining in ATDC5 cells.BNTA (0.01-10 μM; 6 h) upregulates the expression levels of ECM-related genes COL2A1, ACAN, proteoglycan 4 (PRG4), and SRY-box 9 (SOX9) in human OA chondrocytes.BNTA (0.01-10 μM; 6 h) increases Col2a1, Acan, Prg4, and Sox9 mRNA levels, with maximum effects around 0.1 μM in IL1β-induced rat OA chondrocytes.BNTA (0.01-1 μM; 2 or 3 w) enhances anabolism and inhibited inflammatory response in osteoarthritis cartilage explants. Cell Viability Assay Cell Line: Human OA chondrocytes
BNTA (0.015-1.5 mg/kg; intra-articular injection; twice a week for 4 and 8 weeks) could attenuate OA progression developed after anterior cruciate ligament transection (ACLT) in rats. Animal Model: Male SD rats weighing 80 g are induced by ACLT
. Shi Y, et, al. A small molecule promotes cartilage extracellular matrix generation and inhibits osteoarthritis development. Nat Commun. 2019 Apr 23; 10(1): 1914.