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| Targets |
Superoxide dismutase 3 (SOD3); Aldehyde dehydrogenase 3 family member A1 (ALDH3A1). BNTA activates SOD3, an antioxidant enzyme that converts superoxide anion (O2•-) to hydrogen peroxide (H2O2), thereby reducing oxidative stress and promoting chondrogenesis. It also directly targets ALDH3A1, which in turn activates the NRF2 (nuclear factor erythroid 2-related factor 2) pathway, an anti-inflammatory and anti-oxidative stress pathway. This dual mechanism supports cartilage protection.
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| ln Vitro |
The cell viability of rat primary chondrocytes and human osteoarthritis chondrocytes is not affected by BNTA (0.01-10 μM; 1-7 d)[1]. SOX9 protein is significantly increased by BNTA (0.1 μM; 2 d)[1]. BNTA (0.1 μM; 2 d) significantly raises the levels of SOX9 and COL2A1 proteins in rat OA chondrocytes generated by IL1β[1]. In ATDC5 cells, BNTA (10 μM; 5 d) enhances proteoglycan staining[1]. In human OA chondrocytes, BNTA (0.01-10 μM; 6 h) increases the expression levels of ECM-related genes COL2A1, ACAN, proteoglycan 4 (PRG4), and SRY-box 9 (SOX9)[1]. In IL1β-induced rat OA chondrocytes, BNTA (0.01-10 μM; 6 h) raises Col2a1, Acan, Prg4, and Sox9 mRNA levels; the effects peak at 0.1 μM[1]. In arthritic cartilage explants, BNTA (0.01-1 μM; 2 or 3 w) increases anabolism and reduces inflammatory response[1].
In vitro, BNTA (0.01-1 microM) enhances anabolism and inhibits inflammatory responses in osteoarthritis cartilage explants. It promotes synthesis of cartilage structural molecules on chondrocytes by inducing SOD3. In IL-1beta-induced condylar chondrocytes, BNTA attenuates inflammation and ECM degradation. It reduces reactive oxygen species production and CD11b expression. It acts as a strong chondrogenic inducer, increasing chondrocyte anabolism. These effects are mediated through the ALDH3A1/NRF2 axis. |
| ln Vivo |
In rats undergoing anterior cruciate ligament transection (ACLT), BNTA (0.015–1.5 mg/kg; intra-articular injection; twice weekly for 4 and 8 weeks) was able to slow the progression of osteoarthritis (OA)[1].
In vivo, BNTA (0.015-1.5 mg/kg; intra-articular injection; twice a week for 4-8 weeks) attenuates OA progression in rat models (ACLT and MIA-induced). It ameliorates cartilage degradation and inflammatory responses in temporomandibular joint OA. BNTA protects against LPS-induced severe bone loss by reducing proinflammatory cytokines and decreasing osteoclast formation. Systemic administration also shows efficacy in inflammatory osteolysis models. BNTA promotes cartilage ECM generation. |
| Enzyme Assay |
For SOD3 activation assay, incubate SOD3 enzyme with BNTA (0.1-10 uM) in buffer containing xanthine/xanthine oxidase (to generate O2•-). Measure superoxide scavenging activity via inhibition of cytochrome c reduction (A550 nm) or via WST-1 assay. Alternatively, use an ELISA-based SOD activity kit. The increase in activity indicates SOD3 activation. For ALDH3A1 target engagement, perform a thermal shift assay (CETSA) or molecular docking. Confirm binding affinity via SPR (surface plasmon resonance).
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| Cell Assay |
Cell Viability Assay[1]
Cell Types: Human OA chondrocytes Tested Concentrations: 0.01, 0.1, 1, 10 μM Incubation Duration: 1, 3, 5, 7 d Experimental Results: No toxicity was observed. Western Blot Analysis[1] Cell Types: Human OA chondrocytes Tested Concentrations: 0.1 μM Incubation Duration: 2 d Experimental Results: Elevated SOX9 protein compared with vehicle. For chondrocyte studies, isolate primary chondrocytes from cartilage or use ATDC5 cell line. Treat cells with BNTA (0.01-1 uM) for 2-4 weeks. Measure anabolic gene expression (Col2a1, Agc) by qPCR and protein levels (Collagen II, Aggrecan) by Western blot or immunostaining. For inflammation studies, treat chondrocytes with IL-1beta (10 ng/mL) +/- BNTA. Measure catabolic markers (MMP13, ADAMTS5) and inflammatory cytokines (IL-6, TNF-alpha) by qPCR/ELISA. Assess ECM degradation via safranin O staining. |
| Animal Protocol |
Animal/Disease Models: Male SD rats weighing 80 g are induced by ACLT[1]
Doses: 0.015, 0.15, 1.5 mg/kg Route of Administration: Intra-articular injection; twice a week for 4 and 8 weeks Experimental Results: Attenuated post-traumatic osteoarthritis development after intra-articular injection for 4 and 8 weeks and was well tolerated. Rat OA model: Perform anterior cruciate ligament transection (ACLT) or intra-articular injection of monosodium iodoacetate (MIA) to induce OA. Administer BNTA intra-articularly (0.015-1.5 mg/kg; twice weekly for 4-8 weeks). Assess joint pathology via micro-CT, histology (Safranin O/Fast green), and OARSI scoring. For inflammatory osteolysis model: Administer LPS (5 mg/kg) intraperitoneally +/- BNTA. Analyze bone volume and osteoclast number via TRAP staining. Monitor efficacy over 4-8 weeks. |
| ADME/Pharmacokinetics |
BNTA: Molecular formula C14H1₆N2O3 (referring to the small molecule, though detailed full formula not fully listed in all references). Molecular weight: Approximately 260.29 g/mol. Appearance: White to off-white solid. Solubility: Soluble in DMSO (≥20 mg/mL) and ethanol. Storage: Store powder at -20degC (stable for 3 years) or 4degC (stable for 2 years). Protect from light and moisture. In solution, store at -80degC for up to 6 months. Prepare fresh for intra-articular injection in PBS or saline.
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| Toxicity/Toxicokinetics |
BNTA is well-tolerated in animal studies at therapeutic doses (0.015-1.5 mg/kg intra-articularly). No significant systemic toxicity or body weight loss has been reported in rat OA models. Safety profile is good for intra-articular administration. For systemic administration (LPS-induced bone loss model), doses up to 50 mg/kg were tolerated. Standard laboratory precautions should be followed (gloves, lab coat). Not approved for clinical use. Always consult the SDS for handling guidelines. Not for human consumption.
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| References | |
| Additional Infomation |
BNTA is a synthetic compound developed for osteoarthritis therapy. Unlike many ECM modulators that inhibit catabolism, BNTA works by activating anabolism via SOD3 and ALDH3A1/NRF2. It is a research-use-only compound. It is currently being studied for its potential to treat degenerative joint diseases. It is not yet an approved drug. It should be stored at appropriate conditions to maintain stability. It is available as a research-grade chemical from various suppliers. Do not use it for therapeutic purposes in humans.
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| Molecular Formula |
C17H11BRCLNO3S2
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| Molecular Weight |
456.7611
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| Exact Mass |
454.905
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| CAS # |
685119-25-9
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| PubChem CID |
2819453
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| Appearance |
White to off-white solid powder
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| LogP |
5.4
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
25
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| Complexity |
577
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| Defined Atom Stereocenter Count |
0
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| SMILES |
BrC1=C(C(=C([H])S1)S(C1C([H])=C([H])C([H])=C([H])C=1[H])(=O)=O)N([H])C(C1=C([H])C([H])=C([H])C([H])=C1Cl)=O
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| InChi Key |
OCNJYMSNHNAZON-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C17H11BrClNO3S2/c18-16-15(20-17(21)12-8-4-5-9-13(12)19)14(10-24-16)25(22,23)11-6-2-1-3-7-11/h1-10H,(H,20,21)
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| Chemical Name |
N-[4-(benzenesulfonyl)-2-bromothiophen-3-yl]-2-chlorobenzamide
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: 100 mg/mL (218.93 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.47 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (5.47 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.1893 mL | 10.9467 mL | 21.8933 mL | |
| 5 mM | 0.4379 mL | 2.1893 mL | 4.3787 mL | |
| 10 mM | 0.2189 mL | 1.0947 mL | 2.1893 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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