AIG01 is a highly potent and selective oral SOS1 inhibitor targeting pan-KRAS cancers, including NSCLC, PDAC, and CRC. By disrupting the SOS1–KRAS interaction, AIG01 blocks KRAS activation and enhances the efficacy of KRAS G12C inhibitors like Sotorasib. It shows strong synergy in KRAS and EGFR mutant models and overcomes acquired resistance in G12C-driven cancers​.

AIG07 is a selective, allosteric USP1 inhibitor designed to treat BRCA-deficient and other HRD-positive tumors. By preventing USP1-mediated deubiquitination of FANCD2 and PCNA, AIG07 disrupts DNA repair pathways, inducing synthetic lethality. It shows potent synergy with PARP inhibitors like Olaparib and addresses a key unmet need in patients resistant to current HRD therapies​.

AIG14 directly targets the active, GTP-bound form of KRAS G12C (“ON” state), aiming to overcome limitations of current inhibitors that rely on trapping the inactive GDP-bound form. By selectively disrupting KRAS signaling in its active state, AIG14 has the potential to deliver deeper and more sustained pathway inhibition, particularly in tumors that rapidly cycle KRAS or develop resistance to conventional G12C inhibitors.

AIG18 inhibits METTL3, an m6A methyltransferase involved in RNA epitranscriptomic regulation. By modulating m6A marks on cancer-relevant transcripts, AIG18 impairs oncogenic RNA processing, stability, and translation. This represents a novel strategy to target cancer-driving gene expression programs post-transcriptionally, with the potential to affect a broad range of tumor types.