P1, N=108, Recruiting, Daiichi Sankyo | Active, not recruiting --> Recruiting

P1, N=108, Active, not recruiting, Daiichi Sankyo | N=78 --> 108 | Trial completion date: Jun 2026 --> May 2030 | Trial primary completion date: Jun 2026 --> May 2030

P1, N=14, Active, not recruiting, Boehringer Ingelheim | Trial primary completion date: May 2026 --> Sep 2026

P1, N=85, Active, not recruiting, Boehringer Ingelheim | Recruiting --> Active, not recruiting

P1, N=48, Active, not recruiting, Boehringer Ingelheim | Recruiting --> Active, not recruiting

P1, N=90, Recruiting, Boehringer Ingelheim | Trial primary completion date: Oct 2026 --> Aug 2027

LM-101 was well tolerated. The preliminary efficacy signal supports further evaluation of LM-101 plus rituximab in relapsed/refractory lymphoma.

In vivo, RRx-001 significantly inhibits tumor growth, enhances T-cell infiltration, promotes M1 macrophage polarization, downregulates PD-L1 expression, and strengthens anti-tumor immunity through T cell-related pathways. With both metabolic and immunomodulatory effects, RRx-001 provides a basis for novel HCC therapies, and future research could explore its synergistic effects with immune checkpoint inhibitors.

Nanoprodrugs orchestrate a sophisticated cascade of immune activation through four synergistic mechanisms: 1) size-switchable disassembly upon glutathione/ cholesterol exposure for deep tumor penetration; 2) redox imbalance driven by reactive nitrogen species accumulation and glutathione depletion via the synergistic action of oxaliplatin, ferrocene, and RRx-001 for ferroptosis augmentation; 3) immunogenic cell death induction via ferroptosis-apoptosis to initiate tumor immunity cycle, promoting T cell infiltration; and 4) T cell function reinvigoration with the downregulation of programmed cell death protein 1 and T-cell immunoglobulin 3 expression through cholesterol depletion in TME. This integrated approach achieved primary and distant tumor growth suppression, established durable immune memory against recurrence, and systemically enhanced the antitumor immunity. By concurrently targeting tumor immunogenicity, TME immunosuppression, and T cell exhaustion, this multidimensional strategy represents a transformative advancement in cancer immunotherapy.

In conclusion, this study systematically characterizes the clinical and immunological associations of CD47 across multiple cancers and highlights its potential role in pancreatic adenocarcinoma, supporting the further investigation of CD47 as a therapeutic target.

P2, N=28, Completed, Boehringer Ingelheim | Active, not recruiting --> Completed

P1, N=14, Active, not recruiting, Boehringer Ingelheim | Recruiting --> Active, not recruiting