Chemical Structure : ADT-007
CAS No.: 1945941-09-2
货号: PC-21775Not For Human Use, Lab Use Only.
ADT-007 (ADT007) is a potent, specific pan-RAS inhibitor, shows potential to circumvent resistance to mutant-specific KRAS inhibitors and activates antitumor immunity.
规格 | 价格 | 库存 | 数量 |
---|---|---|---|
5 mg | ¥2280 | In stock | |
10 mg | ¥3580 | In stock | |
25 mg | ¥5880 | In stock | |
50 mg | Get quote | ||
100 mg | Get quote |
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ADT-007 (ADT007) is a potent, specific pan-RAS inhibitor, shows potential to circumvent resistance to mutant-specific KRAS inhibitors and activates antitumor immunity.
ADT-007 displays high potency and selectivity to inhibit the growth of KRAS G13D HCT-116 cells with an IC50 of 5 nM, 100 fold less sensitive to RAS WT HT-29 cells.
ADT-007 displays potency in KRAS G12C MIA PaCa-2 PDA cells, resulting in IC50 values as low as 2 nM and a selectivity index approaching 1200-fold relative to RAS WT BxPC-3 PDA cells.
ADT-007 also potently inhibits the growth of three other mutant KRAS PDA cell lines with G12V or G12D mutations.
ADT-007 suppresses MIA PaCa-2 cells growth in 2D monolayer and 3D spheroid cultures with IC50 values of 2.1 and 3.3 nM, respectively.
ADT-007 completely inhibits colony formation of PDA cell lines with G12C, G12D, and G12V KRAS mutations, whereas colony formation of RASWT 136 BxPC-3 cells is not significantly affected.
ADT-007 inhibits activated RAS and downstream MAPK/AKT signaling in human CRC and PDA cell lines.
ADT-007 exhibited 10x greater potency than AMG-510 in growth assays involving parental mutant KRAS G12C MIA PaCa-2 cells, also potently inhibits Lewis lung cancer (LLC) cells (NRAS Q61H) growth with IC50 of 9 nM.
ADT-007 preferentially binds nucleotide-free RAS, inhibit RAS-driven cancer cell growth, activated RAS levels, and MAPK/AKT signaling.
分子量 | 449.48 | |
分子式 | C26H24FNO5 | |
外观性状 | Solid | |
储存条件 |
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Solubility |
10 mM in DMSO |
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Chemical Name/SMILES |
(1Z)-5-Fluoro-N-(2-furanylmethyl)-1-[(4-hydroxy-3,5-dimethoxyphenyl)methylene]-2-methyl-1H-indene-3-acetamide |
1. Jeremy B Foote, et al. bioRxiv. 2024 Jan 24:2023.05.17.541233.
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