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.

P1, N=6, Recruiting, City of Hope Medical Center | Trial completion date: Oct 2026 --> Jun 2027 | Trial primary completion date: Oct 2026 --> Jun 2027

Our case provides further evidence supporting the hypothesis of a significant association between immunosuppression and MCC pathogenesis.

We also found that the anti-proliferation activity with both nucleosides was suppressed by the treatment of dipyridamole, a non-selective inhibitor for ENT1 and ENT2, but not nitrobenzylthioinosine, a low inhibitor for ENT2...This suggests that guanosine or 2-deoxyguanosine induces G1 arrest in cancer cells via the activation of C/EBPβ. Encouraged by these promising results, guanosine and 2'-deoxyguanosine show potential applications in cancer prevention.

This study predicted the therapeutic target of IBD and the molecular mechanism of dipyridamole in treating IBD, providing a new direction for the treatment of IBD and a theoretical basis for further research.