hydroxychloroquine

P=N/A, N=186, Recruiting, The Fourth Affiliated Hospital of Zhejiang University School of Medicine | Not yet recruiting --> Recruiting

P=N/A, N=25, Completed, Children's Hospital of Fudan University | Recruiting --> Completed | Trial completion date: Jul 2026 --> Mar 2026

HCQ attenuated CTX-induced cellular senescence, stabilized mitochondrial membranes, decreased reactive oxygen species (ROS) production and mitochondrial DNA (mtDNA) leakage, inhibited the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway, and suppressed the expression of senescence-associated secretory phenotype (SASP) factors. Collectively, our preclinical findings demonstrate that HCQ alleviates CTX-induced POF, which is associated with the mitigation of granulosa cell senescence and modulation of the mtDNA-cGAS signaling pathway.

P2, N=200, Not yet recruiting, Ministry of Health, Saudi Arabia

P2, N=22, Active, not recruiting, Cancer Trials Ireland | Recruiting --> Active, not recruiting

The feasibility of a feeder-free, low-dose IL-2 TIL expansion system was demonstrated. PD-1 blockade significantly enhanced antitumor activity and treatment tolerability, thus supporting its promise as an alternative to high-dose IL-2. HCQ demonstrated potential immunomodulatory effects, although its in vivo benefit was minimal. This strategy warrants further clinical evaluation in solid tumors.

P2, N=30, Not yet recruiting, Assistance Publique - Hôpitaux de Paris

P2, N=50, Completed, Shanghai Children's Hospital | Recruiting --> Completed

The combination of BINI + HCQ demonstrated a challenging toxicity profile and limited clinical activity in patients with chemorefractory metastatic PDAC.

CM@pGGH is synthesized by conjugating GA and hydroxychloroquine (HCQ)-an FDA-approved antimalarial and immunomodulator-to polyglutamic acid (PGA) using disulfide and ester linkages, followed by incorporation of a hybrid membrane derived from tumor cell and macrophage...In vivo, CM@pGGH reprograms the tumor immune microenvironment by repolarizing tumor-associated macrophages to a pro-inflammatory M1 phenotype and promoting CD8+ T-cell infiltration, resulting in significant PANoptosis-driven immunogenic cell death (ICD) and sustained antitumor immunity. These findings highlight a dual-prodrug and immune-reprogramming strategy with potential for treating refractory cancers.

P=N/A, N=90, Not yet recruiting, Sohag University

P4, N=30, Not yet recruiting, Walter and Eliza Hall Institute of Medical Research