| Features: Statin |
Atorvastatin is a statin, i.e., an inhibitor of HMG-CoA reductase, the rate-limiting enzyme of the mevalonate pathway. Clinically it is prescribed to lower LDL cholesterol and cardiovascular risk.Across preclinical and observational contexts, atorvastatin tends to: -DOWNREGULATE proliferative and survival signaling (via impaired prenylation) -REDUCE inflammatory signaling (NF-κB–linked effects) -MODULATE immune and stromal interactions -SENSITIZE some tumors to chemotherapy or radiation (context-dependent)-Epidemiologic studies suggest statin use is associated with reduced incidence or improved outcomes in some cancers (e.g., colorectal, prostate, breast). |
| Features: |
| Dipyridamole is a medication primarily used for its antiplatelet and vasodilatory effects.(cardiovascular)
Dipyridamole is primarily known as a phosphodiesterase inhibitor and anti‐platelet agent. Mechanism: Dipyridamole inhibits phosphodiesterases (PDEs), enzymes that break down cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Cancer Relevance: Increased cyclic nucleotide levels can affect cell proliferation, apoptosis, and differentiation. Elevated cAMP, for example, may contribute to growth arrest or modify signaling cascades in certain cancer cells. • Dipyridamole has been observed in some studies to exert antioxidant effects. • There is evidence—albeit less definitive in some cases—that dipyridamole might influence mitochondrial function, potentially altering the balance between ROS production and detoxification. • By stabilizing mitochondrial membranes or affecting mitochondrial signaling pathways, dipyridamole could reduce the likelihood of excessive ROS generation. Current literature does not provide strong evidence that dipyridamole directly inhibits the mevalonate pathway?? A) Nucleoside Salvage Blockade -Tumors often rely on nucleoside salvage under stress. -Dipyridamole blocks nucleoside uptake → replication stress and DNA synthesis pressure, especially when de novo synthesis is compromised. B) Metabolic Stress & Redox Effects -Interferes with PPP/NADPH support in certain contexts. -Can sensitize cells to oxidative and metabolic stress, tipping stressed tumors toward death. C) Adenosine Signaling Modulation -By altering extracellular/intracellular adenosine handling, dipyridamole can modify immune and stress signaling in the tumor microenvironment (context-dependent). -Chemo-sensitizer (adjunct) Yes (experimental) -Chemopreventive candidate Yes (preclinical/observational) |
| 4985- | ATV, | Dipy, | Repurposing of the Cardiovascular Drug Statin for the Treatment of Cancers: Efficacy of Statin-Dipyridamole Combination Treatment in Melanoma Cell Lines |
| - | in-vivo, | Melanoma, | SK-MEL-28 | - | in-vitro, | BC, | MDA-MB-435 |
| 4986- | ATV, | Dipy, | The combination of statins and dipyridamole is effective preclinically in AML, MM, and breast cancer |
| - | Review, | Var, | NA |
| 4988- | ATV, | Dipy, | Repurposing of the Cardiovascular Drug Statin for the Treatment of Cancers: Efficacy of Statin–Dipyridamole Combination Treatment in Melanoma Cell Lines |
| - | in-vivo, | Melanoma, | NA |
| 4983- | Dipy, | ATV, | Targeting tumor cell metabolism via the mevalonate pathway: Two hits are better than one |
| - | Review, | Var, | NA |
| 4984- | Dipy, | ATV, | Immediate Utility of Two Approved Agents to Target Both the Metabolic Mevalonate Pathway and Its Restorative Feedback Loop |
| - | in-vitro, | AML, | NA |
| 4987- | Dipy, | ATV, | Enhanced cardioprotection against ischemia-reperfusion injury with a dipyridamole and low-dose atorvastatin combination |
| - | in-vivo, | Nor, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:2 Target#:% State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid