P1/2, N=15, Not yet recruiting, SoVarGen Co., Ltd.

P2, N=28, Recruiting, University Hospital, Lille | Trial completion date: Feb 2025 --> Feb 2026 | Trial primary completion date: Feb 2025 --> Feb 2026

Together, our findings revealed shared molecular features across MPN and AML, identified a prognostic gene signature for risk stratification, and provided rationale for PI3K/mTOR inhibition as a promising therapeutic strategy in myeloid malignancies.

Importantly, multiomics analyses reveal a unique mechanism of action: APT NPs induce the upregulation of the stress-responsive gene DNA damage-inducible transcript 4 (DDIT4), which inhibits the mammalian target of the rapamycin complex 1 (mTORC1) signaling pathway...In vivo, the MCF-7 tumor-bearing mouse model confirms potent antitumor efficacy without significant side effects. This work not only introduces a hypoxia-insensitive PDT agent but also provides novel insights into the mechanistic interaction between transcriptional and metabolic regulation in PDT, highlighting the potential of AIE-active materials for cancer therapy.

P1, N=5, Recruiting, Xuanwu Hospital, Beijing | Initiation date: Nov 2025 --> Mar 2026

P2, N=106, Active, not recruiting, University of Wisconsin, Madison | Recruiting --> Active, not recruiting | Trial completion date: Dec 2026 --> Sep 2026 | Trial primary completion date: Dec 2025 --> Sep 2026

P2/3, N=60, Active, not recruiting, University of Chicago | Recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

We discovered that BEX2 promotes autophagic flux via PI3K/AKT/mTOR signaling. BEX2 interacts with PIK3CA and impairs PIK3CA and p85 interaction, which hinders activation of PI3K/AKT/mTOR signaling and promotes autophagy induction.

The mechanistic target of rapamycin complex 2 (mTORC2) signaling pathway, which regulates cell growth and migration, exhibits oncogenic function in colorectal cancer (CRC)...In immunodeficient mice CRC xenografts, SLAP depletion enhanced mTORC2 activity and sensitized CRC cells to mTOR catalytic inhibitors. Together, our findings reveal a previously unrecognized SLAP-UBE3C-mLST8 axis that regulates mTORC2 integrity and suggest a potential therapeutic avenue for targeting mTORC2 in CRC.

Co-inhibition of mTOR or the SLC3A2/SLC7A5 complex using dactolisib or JPH203 restores sensitivity to KRAS inhibitors in vitro and in vivo. These findings support combinatorial targeting of mTOR signaling or amino acid transport to overcome intrinsic resistance in KRAS-mutant lung cancer.

P3, N=701, Active, not recruiting, Celcuity Inc | Recruiting --> Active, not recruiting | Trial primary completion date: Jun 2025 --> Jun 2026

P=N/A, N=300, Active, not recruiting, Carelon Research | Recruiting --> Active, not recruiting