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RMC5127
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Catalog No. T204085
Alias RMC 5127
RMC5127 is an oral and mutation-selective inhibitor of RASG12V (ON) that inhibits the GTP-bound (ON) form of RAS G12V through the formation of a high-affinity triplex with central nervous system (CNS) permeability and brain permeability. RMC5127 inhibits RAS pathway activity in vitro in KRAS G12V mutant human cancer cells and cellular proliferation, and antitumor activity in preclinical intracranial xenograft models and subcutaneous CDX and PDX models of KRAS G12V mutant NSCLC, PDAC and CRC.
RMC5127
😃Good
Catalog No. T204085Alias RMC 5127
RMC5127 is an oral and mutation-selective inhibitor of RASG12V (ON) that inhibits the GTP-bound (ON) form of RAS G12V through the formation of a high-affinity triplex with central nervous system (CNS) permeability and brain permeability. RMC5127 inhibits RAS pathway activity in vitro in KRAS G12V mutant human cancer cells and cellular proliferation, and antitumor activity in preclinical intracranial xenograft models and subcutaneous CDX and PDX models of KRAS G12V mutant NSCLC, PDAC and CRC.
| Pack Size | Price | Availability | Quantity |
|---|---|---|---|
| 1 mg | $396 | 10-14 weeks | |
| 5 mg | $993 | 10-14 weeks | |
| 10 mg | $1,590 | 10-14 weeks | |
| 25 mg | $3,360 | 10-14 weeks | |
| 50 mg | $4,970 | 10-14 weeks |
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Product Introduction
Bioactivity
Chemical Properties
| Description | RMC5127 is an oral and mutation-selective inhibitor of RASG12V (ON) that inhibits the GTP-bound (ON) form of RAS G12V through the formation of a high-affinity triplex with central nervous system (CNS) permeability and brain permeability. RMC5127 inhibits RAS pathway activity in vitro in KRAS G12V mutant human cancer cells and cellular proliferation, and antitumor activity in preclinical intracranial xenograft models and subcutaneous CDX and PDX models of KRAS G12V mutant NSCLC, PDAC and CRC. |
| In vitro | RMC5127 drove deep suppression of RAS pathway activity, inhibited cell proliferation, and induced apoptosis in a panel of KRASG12V mutant human cancer cells in vitro but only caused submaximal inhibition in the panel of K/N/HRAS wildtype cancer cells, indicative of selectivity for KRASG12V over K/N/HRAS wildtype[1]. |
| In vivo | RMC5127 showed profound and durable anti-tumor activity in vivo in multiple KRASG12V-mutant cancer models, including subcutaneous CDX and PDX models of NSCLC, pancreatic cancer (PDAC), and colorectal cancer (CRC).RMC5127 also demonstrated brain penetration, with dose-dependent exposure in whole brain tissue of naïve mice. In an intracranial xenograft model of KRASG12V-mutant tumors, RMC5127 achieved comparable brain tumor drug exposure, induced strong pharmacodynamic effects, and drove significant tumor regression at well-tolerated doses[1]. |
| Alias | RMC 5127 |
| Molecular Weight | 1062.32 |
| Formula | C57H75N9O9S |
| Relative Density. | no data available |
Storage & Solubility Information
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
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(mother liquor concentration of 40 mg/mL), if you need to configure a concentration that exceeds the solubility of the product, please contact us first.Preparation method for in vivo formula: Take 50 μL DMSO main solution, add 300 μLPEG300 mix well and clarify, then add 50 more μL Tween 80, mix well and clarify, then add 600 more μLSaline/PBS/ddH2O mix well and clarify
main solution, add 300 μLPEG300 mix well and clarify, then add 50 more μL Tween 80, mix well and clarify, then add 600 more μLSaline/PBS/ddH2O mix well and clarifyFor Reference Only. Please develop an appropriate dissolution method based on your laboratory animals and route of administration.
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