These findings confirm Dipyr's protective potential against Cyc-induced hepatotoxicity mainly via antioxidant and anti-inflammatory mechanisms. Dipyr may probably mitigate hepatic injuries when used as an adjuvant in patients undergoing Cyc therapy.

P2, N=90, Recruiting, Stanford University | Not yet recruiting --> Recruiting | Trial completion date: Mar 2026 --> May 2027 | Trial primary completion date: Mar 2026 --> May 2027

We also found that PPARγ activators, ciglitazone and pioglitazone, significantly inhibited the TGF-α-induced migration of HuH7 cells. Cilostazol and dipyridamole also inhibited the activation of AKT but not EGFR. Taken together, these results strongly suggest that cilostazol and dipyridamole inhibit TGF-α-induced HCC cell migration by suppressing the AKT pathway through PPARγ activation.

Here, we describe a novel DHODH inhibitor, JNJ-74856665, that showed strong efficacy in a subset of AML samples. The transcriptional regulator SREBF2, known to control cholesterol and lipid metabolism, was upregulated in DHODHi sensitive AMLs, and a strong synergy was observed between combination of both DHODHi and the SREBP inhibitor dipyridamole. Our data indicate that combined DHODH and SREBP inhibition is of interest to explore further as a therapeutic target option in AML.

Pharmacologic inhibition of AMP-metabolizing pathway by Pentostatin activates muscle AMPK, confers resistance to obesity and improves metabolic health. These findings identify an enhancer regulator limiting AMPK-mediated muscle fuel catabolism, offering a potential strategy for treating obesity-related disorders.

This case emphasizes that KDSS with leukemoid reaction may mimic hematologic malignancy, delaying appropriate immunomodulatory therapy. Extreme leukocytosis (≥70 × 109/L) should not exclude KDSS, especially in children with unexplained fever and shock. Early recognition, adjunctive corticosteroid therapy, and individualized anticoagulation strategies are critical to prevent misdiagnosis and improve outcomes.

To address the suboptimal treatment outcomes in these patients, we identified PYR-41 and pentostatin as potential therapeutic agents, which are anticipated to enhance therapeutic efficacy in the high-risk group. Additionally, four biomarkers (HSPA1A, CHDH, TRAP1, CDC25C) were validated by quantitative real-time PCR, with significant expression differences between normal intestinal epithelial cells and colon cancer cells. Our prognostic model provides accurate CRC outcome prediction and guides personalized therapeutic strategies.

Classical hairy cell leukemia (HCL-c) is very sensitive to the standard of care with purine nucleoside analogs (PNAs) cladribine (cDa) and pentostatin. We conclude that BAFF provides chemo-protection in HCL-v cells by activating nonclassical NF-κB signaling, which results in the upregulation of multiple pro-survival or anti-apoptotic genes. Our results highlight an important role of BAFF in HCL-v resistance to chemotherapy and suggest that the BAFF blockade may enhance the chemosensitivity to PNAs in drug-resistant HCL-v patients.

DIP in combination with IVIG and ASP significantly enhances treatment efficacy and improves levels of antiplatelet aggregation factors and inflammatory markers in children with KD.

P2, N=90, Not yet recruiting, Stanford University

Dipyridamole alleviated experimental periodontitis in rat models by regulating M1 polarization via activation of PKA/PKG pathways and emerges as a hopeful remedy for periodontitis.

Therefore, this strategy can have significant potential in the prevention of tumor metastases and recurrence. To the best of our understanding, this study represents a pioneering showcase of tumor pyroptosis, induced by glycolytic inhibitors, which can be effectively coordinated with DIP-mediated TAM polarization for immune activation, offering a new paradigm for differentially sustained drug delivery to foster cancer immunotherapy.