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서브 비주얼 서브 비주얼

Rapidly Advancing
AI-Built Next-Generation
Therapies

  • Potential Indications

    Potential IndicationsEarly Stage

    Early StageLead Optimization

    Lead OptimizationCandidate Selection

    Candidate SelectionIND-Enabling

    IND-Enabling

  • AIGEN Sciences Owned

  • SOS1
    NSCLC,
    PDAC, CRC
    plusicon

    NSCLC, PDAC, CRC

    AIG01 plusicon

  • 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​.

  • USP1
    BRCA1 Deficient Solid Cancerplusicon

    BRCA1 Deficient
    Solid Cancer

    AIG07 plusicon

  • 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​.

  • PARG
    BRCA1 Deficientplusicon

    BRCA1 Deficient
    Solid Cancer

    AIG13

    plusicon

  • AIG13 targets Poly(ADP-ribose) glycohydrolase (PARG), a key enzyme in DNA damage recovery. By inhibiting PARG, AIG13 disrupts the balance of PARylation dynamics essential for effective DNA repair, inducing synthetic lethality in homologous recombination-deficient tumor cells. This approach offers a mechanistically distinct alternative to PARP inhibition, with potential to overcome or bypass PARP resistance mechanisms.

  • KRAS (G12C ON)
    NSCLC, PDAC, CRCplusicon

    NSCLC, PDAC, CRC

    AIG14

    plusicon

  • 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.

  • METTL3
    Cancerplusicon

    Cancer

    AIG18

    plusicon

  • 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.

  • Undisclosed 10 Targets
    Undisclosed

    Undisclosed

    Undisclosed Multiple Stages

  • Partnered Programs

  • Payload - Linker ADC
    Undisclosed

    Undisclosed

    Undis
    closed

  • Undisclosed 3 Targets
    Undisclosed

    Undisclosed

    Undisclosed

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