| Name | (S)-AMG-510 |
| Description | (S)-AMG-510 is the S-type compound of AMG-510 (Sotorasib), which effectively and selectively inhibits KRASG12C through covalent interaction with mutant cysteine, thereby promoting clinical efficacy in KRASG12C tumors. |
| In vitro | METHODS: KRAS G12 mutant NSCLC cell lines (NCI-H358 [G12C], NCI-H23 [G12C], NCI-H2122 [G12C], A549 [G12S], NCI-H2009 [G12A], NCI-H441 [G12V], and SK-LU1 [G12D]) were treated with (S)-AMG-510 (0.001-100000nM, 72 hours), and cell viability was detected by CCk8.
RESULTS All non-G12C cell lines were as expected. Among KRAS G12 C cells, H358 and H2122 were sensitive, but H23 cells were resistant to (S)-AMG-510.
METHODS: Engineered Ba/F3 cells carrying KRAS G12C were treated with (S)-AMG-510 (0.001-100000nM, 72 hours), and cell viability was determined by CCK8.
RESULTS Ba/F3 cells expressing KRAS G12C were sensitive to sotorasib with an IC50 value of 12.4nM.
METHODS: Ba/F3 cells expressing KRAS G12C or G12D were treated with (S)-AMG-510 (10-100nM, 6 hours) or adagrasib and immunoblotted.
RESULTS (S)-AMG-510 inhibited pERK and pS6 levels in Ba/F3 cells expressing KRAS G12C; it had no effect on KRAS G12D. [3] |
| In vivo | METHODS: (S)-AMG-510 (10 mg/kg, oral) or sotorasib (10 mg/kg) + encorafenib (20 mg/kg) were used to treat NOD/SCID mice bearing tumor xenografts. The body weight and tumor size of the mice were monitored every 2 days.
RESULTS (S)-AMG-510 withdrawal and the combination of BRAF inhibitors induced tumor regression in vivo. [4] |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | DMSO : 5.61 mg/mL (10 mM)
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| Keywords | Ras | inhibit | AMG 510 | Sotorasib racemate | (S)-Sotorasib | Inhibitor | AMG-510 | Sotorasib | AMG510 |
| Inhibitors Related | Adagrasib | BI-2493 | CCG-257081 | Ketoconazole | Deltarasin | ZCL278 | MRTX1133 | Salirasib | RMC-6236 | (S)-(-)-Perillyl alcohol | CASIN | Sotorasib |
| Related Compound Libraries | Bioactive Compound Library | Membrane Protein-targeted Compound Library | Anti-Cancer Clinical Compound Library | Inhibitor Library | Anti-Cancer Approved Drug Library | FDA-Approved Drug Library | Bioactive Compounds Library Max | GPCR Compound Library | Anti-Cancer Active Compound Library | Anti-Cancer Drug Library |
United States
