KRAS remains a challenging target in cancer biology because of its high affinity for GTP/GDP and the limited availability of classical druggable pockets. Advances in covalent G12C inhibitors have renewed discovery interest, while diverse KRAS strategies require mechanism-specific assay systems.
Our services support covalent inhibition, upstream exchange-factor modulation, downstream effector blockade and molecular-glue programs with tailored biochemical, biophysical and cell-based study designs.
Our recombinant protein portfolio includes clinically relevant KRAS mutants such as G12C, G12D, G12V, G13D, Q61H, Q61L and A146T, with N-His, C-Avi or N-GST tag formats and truncated or full-length options. SOS1/2 and CRAF are also available to support RAS pathway studies.
All listed assays are based on TR-FRET technology. The table is horizontally scrollable within narrow content areas.
| Target | SOS1/2 PPI | GTP Displacement | cRAF PPI | NEA | Tri-complex | Competitive Binding |
|---|---|---|---|---|---|---|
| KRAS G12D, G12C, WT | Available | Available | Available | Available | Available | Available |
| KRAS G12V, G12A, G12S, G12R | Selected | Selected | Available | Available | Selected | Available |
| KRAS G13C, G13D, Q61H, Q61K, Q61L, Q61R, A146T | Selected | Selected | Available | Available | Selected | Selected |
| KRAS [G12C/Y64H], KRAS [G12D/Y64H] | — | — | Available | Selected | Available | Available |
| HRAS, NRAS | — | — | Available | Available | Available | Available |
PPI: direct interaction of RAS with partners including SOS1, SOS2 or cRAF RBD. NEA: nucleotide exchange assays that evaluate GDP-to-GTP loading.
Tri-complex and competitive binding: molecular-glue-enabled assays that evaluate KRAS–Cyclophilin A complex formation and cRAF effector displacement.
Profile direct KRAS-targeting molecules across mutant forms and nucleotide states.
Characterize molecules that stabilize KRAS–Cyclophilin A interactions and prevent effector binding.
GDP-, GTP-, GMPPNP- and GppNHp-bound proteins can be used to quantify KD, kon/koff and conformational selectivity.
High-resolution intact MS detects protein–inhibitor conjugates and modification ratios.
Multiple inhibitor concentrations and time points can support quantitative kinact/Ki analysis.
Occupancy-based analysis supports SAR exploration, compound ranking and covalent reaction modelling.
Fixed and custom panels cover hotspot mutations such as G12C, G12D, G12V and NRAS across up to 15 tumor types.
Explore KRAS 2D/3D cell panels ↗Cytokine-dependent Ba/F3 KRAS models provide a tractable setting for potency and resistance-mechanism studies.
Explore Ba/F3 cell-line screening ↗Validated CDX libraries across multiple cancer types can support custom model establishment and efficacy evaluation.
Explore in vivo CDX models ↗We value your inquiries and are here to provide you with tailored solutions for your drug discovery and development needs. Whether you have questions, require more information, or are interested in discussing potential collaborations, our team of experts is just a message away.
Feel free to reach out to us.
Address: Bldg 16, Yd 18, Kechuang 13th St, Etown, Tongzhou Dist, Beijing, 100176, China
Email: marketing@ice-biosci.com
Tel：+86-10-67809840
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