A study recently published in the journal Cancer Research reports that sildenafil, the active ingredient in Viagra, may restrict cancer cells’ ability to metastasize by disrupting their cholesterol processing.
The research, led by scientists at the Weizmann Institute of Science in Israel and co-authored by investigators from the U.S. National Cancer Institute, drew on laboratory experiments, animal models, human cancer cell cultures, and an analysis of health records.
The National Cancer Institute announced the findings in late July 2026, stating that early research co-authored by its investigators suggests sildenafil “may disrupt how tumor cells process cholesterol, reducing their ability to migrate and form tumors elsewhere in the body.”
The agency noted the results come from laboratory and animal studies plus patient health records linking sildenafil use, particularly with statins, to improved survival, while emphasizing that more research is needed to determine whether the approach can safely and effectively prevent metastasis in people.
Study Findings and Mechanism
Researchers led by Dr. Yarden Ariav in the laboratory of Prof. Ayelet Erez found that PDE5a inhibitors, including sildenafil, induced lysosomal cholesterol accumulation in multiple mouse and human cancer models. This reduced cholesterol bioavailability and impaired cancer cell migration and metastasis. Cancer cells showed heightened sensitivity because of reduced lysosomal gene expression.
Elevated levels of the signaling molecule cGMP, resulting from PDE5a inhibition, bound the lysosomal cholesterol transporter NPC1 and impaired cholesterol export. The resulting depletion disrupted membrane lipid rafts and mitochondrial bioenergetics, limiting metastatic capacity.
Compensatory activation of SREBP2 increased cholesterol synthesis. Combining sildenafil with statins produced additive antimetastatic effects by blocking both lysosomal cholesterol export and biosynthesis.
Analysis of digital health records from approximately 5 million members of Clalit Health Services in Israel showed significantly improved survival among sildenafil users, with a dose-dependent additive benefit when combined with statins. The observational analysis included data on tens of thousands of male cancer patients.
Primary tumor growth was generally unaffected in models, while metastatic burden decreased.
“We have uncovered a new biological pathway that links a well-known signaling molecule to cholesterol regulation within cells, and shown how this pathway can be harnessed to interfere with the ability of cancer cells to form metastases,” Erez said in a Weizmann Institute statement.
Ariav added that “We showed in our research that sildenafil inside cancer cells causes cholesterol to become less available for the cancer cells to metastasise – to generate new energy and to move from one place to another. It means the cancer cells cannot utilise this cholesterol for their needs.”
Background on Sildenafil and Viagra
Sildenafil was originally developed by Pfizer scientists investigating treatments for hypertension and angina. The U.S. Food and Drug Administration approved Viagra (sildenafil citrate) on March 27, 1998, as the first oral medication for erectile dysfunction. The same active ingredient later received approval under the brand Revatio for pulmonary arterial hypertension.
Sildenafil belongs to the class of phosphodiesterase type 5 (PDE5) inhibitors. It works by increasing levels of cyclic GMP, which relaxes smooth muscle and increases blood flow in certain tissues.
Generic Versions and Equivalence
Generic sildenafil contains the same active ingredient, sildenafil citrate, as brand-name Viagra. The FDA requires generic drugs to be bioequivalent to the brand-name reference product, meaning they deliver the same amount of active ingredient at the same rate and produce the same clinical effect.
Generic versions became widely available after the relevant patents expired and are considered therapeutically equivalent for approved uses.
Potential Clinical Use and Timeframe
The study identifies increasing cGMP levels through PDE5a inhibition as a potential strategy to restrict metastasis and provides a mechanistic basis for observed survival associations. However, the findings are from preclinical models and retrospective observational data.
The National Cancer Institute stated that more research is needed to determine whether this approach can safely and effectively prevent metastasis in people.
No large randomized clinical trials testing sildenafil specifically to prevent or treat cancer metastasis in patients have been completed as of the study’s publication. Erez noted the findings are “still far from routine clinical practice” and cautioned against patients seeking the drug for cancer use on their own.
Researchers indicated the results support further investigation into possible repurposing, but no specific timeline for clinical trials or regulatory approval for oncology use has been established.
Provided by Dallas Express
