cordycepin (OVI-123)

Future research should prioritize pharmacokinetic characterization, investigation of combinatorial therapeutic strategies, and pathways toward clinical translation. Intracellular exposure appears to be shaped by two complementary axes: interference with 3'end polyadenylation and ENT1/ENT2-mediated uptake with ADA-catalyzed deamination.

Although apoptosis is eventually induced in TM3 cells, protective autophagy is also activated to mitigate the cytotoxic impact of the combination treatment. This finding may provide a reference for the development of safe therapeutic regimen for Leydig cell tumors.

P2, N=127, Recruiting, Second Affiliated Hospital of Soochow University | Not yet recruiting --> Recruiting

Collectively, COR inhibited MM progression by inducing ferroptosis through upregulating CLEC2. The online version contains supplementary material available at 10.1007/s10616-025-00886-5.

They enhance innate and cell-mediated adaptive immunity not only under normal conditions but also in immunosuppressed states induced by cyclophosphamide, interleukin-4, tumor culture supernatant, methotrexate, cancer cell-line-xenografts, influenza virus, and severe acute respiratory syndrome coronavirus 2. This study reviewed recent and notable literature evaluating the immunomodulatory potentials of CM extract, cordycepin, and polysaccharides. In vitro, in vivo, and clinical trial results indicate that CM is safe for administration and shows promise for developing functional foods having various efficacies such as immunomodulation, anti-tumor, and neuroprotection.

CS alleviates COPD symptoms by suppressing inflammation, apoptosis, and oxidative stress, suggesting novel therapeutic strategies.

Natural compounds (neferine, ajoene, baicalein, isoliensinine, curcumin analogs) and synthetic drugs (5-FU, oxaliplatin, irinotecan, norcantharidin, cordycepin) modulate EMT and trigger ferroptosis, cuproptosis, paraptosis, and autophagy...Simultaneous targeting of EMT, CR-CSC maintenance, and chemoresistance using multifunctional natural and synthetic agents represents a promising strategy in CRC therapy. Induction of alternative cell death pathways may improve response, minimize relapse, and enable combinatorial regimens for resistant tumors.

Recent advancements in improving cordycepin's biostability, bioavailability, and transport efficiency within the body system have further supported the clinical application of this compound in medical oncology. This review highlights key research findings and explores promising future directions with the aim of contributing to ongoing studies in cancer management.

In conclusion, PDT combined with cordycepin enhances the anti-cancer effect through the PI3K/AKT/FOXO3 signaling pathway in EC cells. The experiment provides a theoretical basis for the combination of PDT and cordycepin to become a new strategy which may increase the efficacy of PDT in esophageal cancer.

Network pharmacology analysis identified 31 potential targets of cordycepin in fibrosarcoma, with its effects on Akt1 (protein kinase B) and disruption of protein phosphorylation pathways emerging as key mechanisms underlying its therapeutic efficacy. Western blot analysis further confirmed that cordycepin simultaneously downregulated both the expression and phosphorylation levels of Akt in a dose-dependent manner.

Furthermore, cordycepin reduced the protein level of phosphorylated EGFR and upregulated the protein expression of Nrf2, NQO1 and HO-1 in the spleens of immunosuppression mice. In conclusion, this study demonstrated that cordycepin ameliorated CTX-induced immunosuppression of mice by reversing metabolic dysfunction and activating Nrf2 pathway through regulating EGFR, indicating its potential as a therapeutic agent for immunosuppression.

In conclusion, Cor provides cardiac protection by inhibiting ACR-induced Nrf2/HO-1 and Bax/Bcl2 signaling failure, hence maintaining heart function. These findings suggest that Cor could be a promising treatment candidate for reducing ACR-induced cardiac damage.