# Daraxonrasib mechanism figure

A. Pancreatic tumor microenvironment, rendered for tissue context. B. Active RAS at the cytoplasmic membrane face and downstream signaling context. C. Experimental tri-complex based on PDB 9BG6: KRAS G12V, cyclophilin A and daraxonrasib. D. Effector blockade and promoted GTP hydrolysis, shown as a distinct explanatory schematic.

The 9BG6 structure contains GNP, a GTP analogue. The structure is not a hydrolysis trajectory; its GNP is not depicted as hydrolyzing. The GTP to GDP + Pi transition in panel D represents the prescribing-information mechanism. Tissue layout, environmental context and animated molecular approach are explanatory, not experimentally measured kinetics. Static coordinates establish a binding arrangement, not transport, affinity or clinical response. Molecular surfaces use a 128-cell Marching Cubes field from 9BG6 atom centers, element-aware radii plus a 1-angstrom display probe, and a 0.14 coordinate scale. These are smoothed display envelopes, not electron-density maps or molecular-dynamics results. The effector, membrane anchor and GTP/GDP reaction objects are schematic; the deposited GNP is not transformed. Tumor-cell loss is an authored scenario, not an estimated response probability.

Sources: [RASONQUE PI, August 2026, Section 12.1](https://www.revmed.com/wp-content/uploads/2026/08/rasonque-pi.pdf); [RCSB PDB 9BG6](https://www.rcsb.org/structure/9BG6).

Independent Cellular Stories scientific communication example, not commissioned or endorsed by Revolution Medicines.