| Identification | Back Directory | [Name]
7H-Pyrazolo[3,4-d]pyridazin-7-one, 4-amino-1,6-dihydro-1-[(3R)-1-(1-oxo-2-propen-1-yl)-3-piperidinyl]-3-(4-phenoxyphenyl)- | [CAS]
1858206-76-4 | [Synonyms]
BTK inhibitor 17
7H-Pyrazolo[3,4-d]pyridazin-7-one, 4-amino-1,6-dihydro-1-[(3R)-1-(1-oxo-2-propen-1-yl)-3-piperidinyl]-3-(4-phenoxyphenyl)- | [Molecular Formula]
C25H24N6O3 | [MDL Number]
MFCD34167515 | [MOL File]
1858206-76-4.mol | [Molecular Weight]
456.5 |
| Chemical Properties | Back Directory | [density ]
1.40±0.1 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
DMSO : 100 mg/mL (219.06 mM; Need ultrasonic) | [form ]
Solid | [pka]
8.00±0.40(Predicted) | [color ]
White to off-white | [InChIKey]
QUYXPVXTKPTPCA-QGZVFWFLSA-N | [SMILES]
C1(=O)NN=C(N)C2C(C3=CC=C(OC4=CC=CC=C4)C=C3)=NN([C@@H]3CCCN(C(=O)C=C)C3)C1=2 |
| Hazard Information | Back Directory | [Uses]
BTK inhibitor 17 is a potent and orally active irreversible BTK inhibitor with an IC50 of 2.1 nM. BTK inhibitor 17 can be used for rheumatoid arthritis research[1]. | [Biological Activity]
BTK inhibitor 17 is a potent and orally active irreversible BTK inhibitor with an IC50 of 2.1 nM. BTK inhibitor 17 can be used for rheumatoid arthritis research[1].
BTK inhibitor 17 (compound 8) could covalently bind to Cys481 and formed an HB network with hinge key residues Met477, Glu475, and gatekeeper Thr474[1].
BTK inhibitor 17 (compound 8; 3-10 mg/kg; oral gavage; daily; for 28 days) treatment inhibits the significant progression of the disease and exhibits a clear dose-dependent reduction per paw clinical scores, and no significant body weight loss is observed for all different dosages[1].BTK inhibitor 17 (compound 8) shows >95% plasma protein binding across three species of human, rat, and mouse. After an intravenous injection, the half-life (rat, 0.32 h; mice, 0.42 h), clearance (rat, 54.6 mL/min/kg; mice, 31.3 mL/min/kg), volume of distribution (rat, 1.55 L/kg; mice, 0.82 L/kg), and AUC exposure (rat, 604 ng.h/mL; mice, 576 ng.h/mL) are observed in two species. After oral administration, BTK inhibitor 17 exhibits higher Cmax (rat, 466 ng/mL; mice, 252 ng/mL) and plasma exposure (rat, 642 ng.h/mL; mice, 128 ng.h/mL) with a favorable oral bioavailability (rat, 23.7%; mice, 11.2%)[1]. | [in vivo]
BTK inhibitor 17 (compound 8; 3-10 mg/kg; oral gavage; daily; for 28 days) treatment inhibits the significant progression of the disease and exhibits a clear dose-dependent reduction per paw clinical scores, and no significant body weight loss is observed for all different dosages[1].
BTK inhibitor 17 (compound 8) shows >95% plasma protein binding across three species of human, rat, and mouse. After an intravenous injection, the half-life (rat, 0.32 h; mice, 0.42 h), clearance (rat, 54.6 mL/min/kg; mice, 31.3 mL/min/kg), volume of distribution (rat, 1.55 L/kg; mice, 0.82 L/kg), and AUC exposure (rat, 604 ng.h/mL; mice, 576 ng.h/mL) are observed in two species. After oral administration, BTK inhibitor 17 exhibits higher Cmax (rat, 466 ng/mL; mice, 252 ng/mL) and plasma exposure (rat, 642 ng.h/mL; mice, 128 ng.h/mL) with a favorable oral bioavailability (rat, 23.7%; mice, 11.2%)[1]. | Animal Model: | Male Balb/C mice injected with collagen[1] | | Dosage: | 3 mg/kg or 10 mg/kg | | Administration: | Oral gavage; daily; for 28 days | | Result: | Inhibited the significant progression of the disease and exhibited a clear dose-dependent reduction per paw clinical scores. |
| [storage]
Store at -20°C | [References]
[1]. Xuejun Zhang, et al. Discovery and Evaluation of Pyrazolo[3,4- d]pyridazinone as a Potent and Orally Active Irreversible BTK Inhibitor. ACS Med Chem Lett. 2019 Dec 11;11(10):1863-1868. |
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InvivoChem
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13549236410 |
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https://www.invivochem.cn/ |
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