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≥98% for sensitive chromatographic and analytical workflows requiring minimal baseline interference.
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Cited in 0 peer-reviewed publications across chromatography, organic synthesis, and cross-coupling reactions.
TK-129 is an orally active, low-toxicity, potent KDM5B inhibitor (with high affinity; IC 50 =44 nM). TK-129 exerts cardioprotective effects by inhibiting KDM5B and blocking the KDM5B -associated Wnt pathway. TK-129 reduces ang II-induced activation of car
Appearance:Solid
IC50& Target:KDM5 44 nM (IC 50 )
In Vitro:TK-129 mediates inhibition of KDM5B activity significantly reduces the activation, migration, and proliferation of myofibroblasts induced by Ang II in vitro. TK-129 (10 μM; 48 h) shows low cytotoxicity in NRCFs and NRCMs. TK-129 (0.1, 0.2, 0.3,
In Vivo:TK-129 (2 g/kg; p.o.; single) shows good bio-safety in mice. TK-129 (50mg/kg; p.o.; twice daily for 24 days) effectively reduces isoproterenol-induced pathological myocardial remodeling in vivo. TK-129 (2 or 10mg/kg; i.v. or p.o.; single) demo
Biological Activity:TK-129 is an orally active, low-toxicity, potent KDM5B inhibitor (with high affinity; IC 50 =44 nM). TK-129 exerts cardioprotective effects by inhibiting KDM5B and blocking the KDM5B -associated Wnt pathway. TK-129 reduces ang II-induced activation of car
| Canonical Smiles | O=C(N[C@H]1CN(C(C2=NNC(C(C)C)=C2)=O)CC1)NC3CC3 |
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| Molecular Weight | 305.38 |
Comprehensive hazard, handling, storage, and regulatory compliance document.
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View spec sheet →| Solubility | DMSO : 100 mg/mL (327.46 mM; Need ultrasonic) |
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