Research by a team of scientists in Israel has found that the erectile dysfunction drug Viagra may be effective in slowing the spread of cancer, reports Healthline. The survival rate was even higher for men who took both Viagra and statins, the study found.
In their findings, published in the journal Cancer Research, the team suggested that Viagra’s active ingredient, sildenafil, shows the potential to interfere with cancer cells’ ability to metastasise and travel around the body.
They said sildenafil accomplishes this feat by blocking cancer cells’ access to cholesterol, a building block that allows tumours to metastasise: they found that male participants who’d used Viagra before being diagnosed with cancer had better overall survival rates than those who hadn’t taken the drug.
Their study did not specify if Viagra would be more effective against certain types of cancers, they added.
“We evaluated the association between pre-cancer diagnosis use and overall survival across a large cohort of cancer patients rather within specific cancer types,” said Samah Hayek, MD, senior epidemiologist at the Clalit Research Institute in Israel and a co-author of the study. “Therefore, we cannot conclude whether the association is stronger for one cancer than another.”
They also did not evaluate whether Viagra could help prevent the spread of cancer in women.
“Our retrospective analysis included mainly men because sildenafil is predominantly prescribed to men,” said Hayek. “As a result, we cannot determine from our clinical data whether a similar association would be observed in women.”
Hayek said that more research, including clinical trials, is needed to determine if Viagra can one day become part of regular cancer treatment.
The study was led by a team from the Weizmann Institute of Science in Israel in collaboration with scientists from Israel’s largest health organisation, Clalit Health Services.
The US National Cancer Institute, as well as physicians and researchers from Clalit’s Beilinson and Hasharon Hospitals, also participated.
Researchers examined laboratory mouse models of cancer and cultures of cancer cells from human subjects. The work was done in co-ordination with scientists from Clalit, who analysed more than 20 years of anonymised medical records from about 5m participants, including an observational study of 40 000 males diagnosed with cancer.
“This study bridges two worlds,” said Hayek. “The laboratory identified a promising biological mechanism, while Clalit’s real-world data showed that the same signal may also be reflected in patient outcomes.”
The researchers reported that they uncovered a previously unknown pathway showing how Viagra’s active ingredient, sildenafil, affects cholesterol regulation inside cells.
Cancer cells depend on cholesterol to detach from primary tumours and invade other organs, and by limiting cholesterol access, sildenafil may make it harder for tumours to spread, they said.
Their findings also suggest that combining sildenafil with statins may further reduce cancer cells’ ability to obtain or produce cholesterol, potentially strengthening the anti-metastatic effect.
They emphasised that the better survival rates were limited to males who had taken Viagra before their cancer diagnosis.
“Our study did not examine whether giving Viagra to patients after they are diagnosed with cancer improves outcomes,” Hayek said. “It looked only at medication use before diagnosis and its association with survival. These findings are encouraging, but they do not mean cancer patients should start taking Viagra.”
Ramin noted that cancer cells can develop “escape mechanisms” to elude certain therapies, so more research is needed to determine how viable a Viagra treatment regimen would be.
Other experts, who were not involved in the study, agreed. “These results are preclinical – meaning the data were derived from cell lines or mice,” said Mike Lattanzi, MD, a medical oncologist and the director of the Genitourinary Cancer Research Programme at Texas Oncology.
“They are intriguing and thought-provoking, but they would need to be validated in human studies to inform the management of cancer patients.”
While Lattanzi emphasised caution, he also expressed some hope.
“One of the reasons this is such an interesting study is that the molecules used to treat the cancer cells are medications many people already take on a daily basis,” he said. “I think it’s certainly plausible that there is a synergistic anticancer effect from the combination of [Viagra and statins].”
“However, I think we’re a long way off from developing any kind of cancer prevention, or so-called chemoprevention strategy, utilising drugs like these to prevent cancer,” he added.
Study details
PDE5a Inhibition Restricts Cancer Metastasis by Disrupting NPC1-Mediated Cholesterol Trafficking Through a Non-canonical cGMP-Dependent Pathway
Yarden Ariav, Samah Hayek, Thomas Cantore et al.
Published in Cancer Research on 14 July 2026
Abstract
Non-canonical metabolic functions of signalling molecules contribute to cancer plasticity and metastatic progression. Here, we demonstrated that PDE5a inhibitors, including sildenafil (Viagra), induced lysosomal cholesterol accumulation across multiple mouse and human cancer models, reducing cholesterol bioavailability and impairing cancer cell migration and metastasis. Cancer cells exhibited heightened sensitivity due to reduced lysosomal gene expression, rendering them particularly vulnerable to disrupted cholesterol trafficking. Mechanistically, elevated cGMP bound the lysosomal cholesterol transporter NPC1, impairing cholesterol export and phenocopying Niemann–Pick type C pathology. The resulting cholesterol depletion disrupted membrane lipid rafts and mitochondrial bioenergetics, thereby limiting metastatic capacity and triggering compensatory SREBP2 activation with increased cholesterol synthesis. Combining sildenafil with statins yields additive antimetastatic effects by concurrently blocking lysosomal cholesterol export and cholesterol biosynthesis. Consistently, analysis of digital health records demonstrated significantly improved survival among sildenafil users, with a dose-dependent additive benefit observed when combined with statins. Together, these findings identify increasing cGMP levels through PDE5a inhibition as a potential strategy to restrict metastasis and offer a potential mechanistic basis for the beneficial effects of sildenafil.
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