BDTX-189
98%
- Product Code: 152593
CAS:
2414572-47-5
| Molecular Weight: | 561.03 g./mol | Molecular Formula: | C₂₉H₂₉CLN₆O₄ |
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| Density: | Storage Condition: | -20°C |
Product Description:
BDTX-189 is a targeted covalent inhibitor designed to selectively inhibit mutant forms of the KRAS protein, particularly KRAS G12C. This mutation is commonly found in non-small cell lung cancer, colorectal cancer, and other solid tumors. By binding irreversibly to the mutated cysteine residue, BDTX-1889 blocks the oncogenic signaling pathways that drive uncontrolled cell growth and tumor progression.
The compound shows high selectivity for the inactive, GDP-bound state of KRAS G12C, locking it in this off state and preventing reactivation. This mechanism leads to sustained suppression of downstream effectors such as MAPK, resulting in reduced tumor cell proliferation and induction of apoptosis in preclinical models.
BDTX-189 is being evaluated in clinical trials for patients with advanced cancers harboring the KRAS G12C mutation. Its oral bioavailability and favorable pharmacokinetic profile support its use in outpatient settings. Early data suggest durable responses in some patients, especially when used as a monotherapy or in combination with other agents like immune checkpoint inhibitors or SHP2 inhibitors.
Due to its precision mechanism, BDTX-189 represents a significant advancement in targeting previously "undruggable" KRAS-driven cancers, offering a promising therapeutic option for a subset of patients with limited treatment alternatives.
Sizes / Availability / Pricing:
| Size | Availability | Price | Quantity |
|---|---|---|---|
| 5mg | 10-20 days | $132.59 |
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BDTX-189
BDTX-189 is a targeted covalent inhibitor designed to selectively inhibit mutant forms of the KRAS protein, particularly KRAS G12C. This mutation is commonly found in non-small cell lung cancer, colorectal cancer, and other solid tumors. By binding irreversibly to the mutated cysteine residue, BDTX-1889 blocks the oncogenic signaling pathways that drive uncontrolled cell growth and tumor progression.
The compound shows high selectivity for the inactive, GDP-bound state of KRAS G12C, locking it in this off state and preventing reactivation. This mechanism leads to sustained suppression of downstream effectors such as MAPK, resulting in reduced tumor cell proliferation and induction of apoptosis in preclinical models.
BDTX-189 is being evaluated in clinical trials for patients with advanced cancers harboring the KRAS G12C mutation. Its oral bioavailability and favorable pharmacokinetic profile support its use in outpatient settings. Early data suggest durable responses in some patients, especially when used as a monotherapy or in combination with other agents like immune checkpoint inhibitors or SHP2 inhibitors.
Due to its precision mechanism, BDTX-189 represents a significant advancement in targeting previously "undruggable" KRAS-driven cancers, offering a promising therapeutic option for a subset of patients with limited treatment alternatives.
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