| Identification | Back Directory | [Name]
Thieno[2,3-c]pyridine-3-carboxamide, 2-[(2-chlorobenzoyl)amino]-6-[[(2-chlorophenyl)amino]thioxomethyl]-4,5,6,7-tetrahydro- | [CAS]
2414916-45-1 | [Synonyms]
ADTL-EI1712
Thieno[2,3-c]pyridine-3-carboxamide, 2-[(2-chlorobenzoyl)amino]-6-[[(2-chlorophenyl)amino]thioxomethyl]-4,5,6,7-tetrahydro- | [Molecular Formula]
C22H18Cl2N4O2S2 | [MOL File]
2414916-45-1.mol | [Molecular Weight]
505.44 |
| Chemical Properties | Back Directory | [density ]
1.556±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
DMF: 1 mg/ml,DMSO: 1 mg/ml,DMSO:PBS (pH 7.2) (1:3): 0.25 mg/ml | [form ]
A crystalline solid | [pka]
11.86±0.20(Predicted) |
| Hazard Information | Back Directory | [Uses]
ADTL-EI1712 is a potent, orally active, and selective dual-target inhibitor of ERK1 and ERK5, inhibition rates of ERK1/5 at 1 μM are 93.54% and 89.35%, respectively. ADTL-EI1712 can induce regulated cell death, a form of cell death that relies on the activation of genetically encoded machinery, to overcome compensatory mechanism in specific cancer cells in vitro and in vivo[1]. | [Biological Activity]
ADTL-EI1712 is a dual inhibitor of ERK1 and ERK5 (IC50s = 40.43 and 64.5 nM, respectively).1 It reduces ERK1 and ERK5 activity by 93.5% and 89.4%, respectively, but also inhibits ERK2 activity by 92.7%, in a panel of 100 kinases at 1 μM. ADTL-EI1712 inhibits proliferation of HL-60 and MKN74, but not HeLa, cancer cells (IC50s = 1.26, 2.55, and >50 μM, respectively). It reduces tumor growth and intratumor phosphorylation of ERK1/2 and ERK5 in an MKN74 mouse xenograft model when administered at a dose of 50 mg/kg per day. | [in vivo]
ADTL-EI1712 (50 mg/kg, PO, once a day for 16 days) significantly inhibits the tumor volume in the xenograft mouse model of HL-60 and MKN-74 cells, while the antitumor effect of HeLa cells group was much weaker[1].
| [storage]
Store at -20°C | [References]
1.Wang, G., Zhao, Y., Liu, Y., et al.Discovery of a novel dual-target inhibitor of ERK1 and ERK5 that induces regulated cell death to overcome compensatory mechanism in specific tumor typesJ. Med. Chem.63(8)3976-3995(2020)
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