Daraxon — Premium RAS API Supplier
The world's first enterprise holding FDA DMF certificate for RMC-6236 | Daraxonrasib, dedicated to innovative drug R&D targeting the RAS pathway
High Purity
Every batch >99% purity, ensuring experimental accuracy
Complete Quality Documentation
Full COA, HPLC, NMR provided
Ample Stock
Ready inventory, fast shipping, bulk customization available
About Daraxon - RAS Pathway Innovation Drug R&D Enterprise
Shanghai Daraxon Bio-Pharmaceutical Co., Ltd. is a high-tech enterprise dedicated to developing innovative drugs targeting the RAS pathway, committed to providing global pharmaceutical companies with high-quality APIs and professional technical services.
As the world's first enterprise holding FDA DMF certificate for Daraxonrasib (RMC-6236) (DMF#43871), we maintain a comprehensive R&D system and strict quality control standards. Our state-of-the-art facilities ensure product purity exceeding 99%, complete documentation including COA, HPLC, and NMR reports, and fast delivery to support your research and development needs.
With our commitment to scientific excellence and regulatory compliance, Daraxon has become a trusted partner for pharmaceutical R&D enterprises worldwide, advancing the frontiers of targeted cancer therapy through reliable, high-quality RAS inhibitor APIs.
Core Product - Daraxonrasib
Daraxonrasib (RMC-6236)
All products are for scientific research or drug registration only. We do not provide products/services for personal use.
Specifications
| CAS Number | 2765081-21-6 |
| Molecular Weight | 811.05 |
| Molecular Formula | C44H58N8O5S |
| Appearance | White to off-white crystalline powder |
| Purity | ≥99% (HPLC) |
| Storage | Solid state: store at low temperature (-20°C, stable for 3 years); Solution: store at -80°C (stable for 6 months) or -20°C (stable for 1 month). |
| Shipping | Room temperature with ice packs |
Daraxonrasib (RMC-6236) is a next-generation, non-covalent RAS(ON) multi-selective inhibitor that targets active RAS-GTP complexes across multiple RAS mutations (G12D, G12V, G12C, Q61H). It demonstrates potent anti-tumor activity by inhibiting downstream MAPK signaling pathway activation.
EC50 values range from 0.1- 3.1 nM across various mutant RAS cell lines, showing superior selectivity and efficacy compared to covalent inhibitors. Clinical studies have demonstrated significant tumor regression in KRAS-mutant solid tumors with manageable safety profile.
In Vitro Activity
- •Mechanism: Binds to switch-II pocket of active RAS-GTP, preventing effector protein interaction
- •Cell Lines: Potent inhibition in KRAS G12D, G12V, G12C mutant pancreatic, colorectal, and NSCLC cell lines
- •pERK Inhibition: >90% reduction in phosphorylated pERK at 100 nM concentration
In Vivo Activity
- •Animal Models: Significant tumor growth inhibition in KRAS-mutant xenograft models (PDX and CDX)
- •Dosage Response: Dose-dependent efficacy observed at 10-50 mg/kg oral administration
- •Combination Therapy: Enhanced efficacy when combined with MEK inhibitors or immunotherapy agents
References
- Jiang J, et al. Translational and Therapeutic Evaluation of RAS-GTP Inhibition by RMC-6236 in RAS-Driven Cancers. Cancer Discov. 2024 Jun 3;14(6):994-1017.
- Patel H V, et al. The farnesyl transferase inhibitor KO-2806 re-sensitizes relapsing tumors to RAS inhibition. BioRxiv, 2024: 2024.12. 20.629824.
- Long SA, et al. Evaluation of KRAS inhibitor-directed therapies for pancreatic cancer treatment. Front Oncol. 2024 May 10;14:1402128.