Viagra may inhibit cancer. Curious, I asked Grok about Cialis:

Yes, there is good reason to expect tadalafil (Cialis) could have a similar anti-metastatic effect, primarily because it is also a selective PDE5 inhibitor.

The recent Weizmann Institute work (published in Cancer Research) shows that sildenafil inhibits PDE5a. This raises intracellular cGMP, which interferes with the lysosomal cholesterol transporter NPC1 via a non-canonical interaction. The result is disrupted cholesterol trafficking/export, lysosomal cholesterol accumulation, impaired membrane lipid rafts and mitochondrial function, reduced energy availability, and decreased ability of cancer cells to migrate and form metastases. Cancer cells appear more sensitive to this than normal cells. Combining with statins (which limit new cholesterol synthesis) enhanced the effect in models, and retrospective patient data linked PDE5 inhibitor use (especially with statins) to better survival.

Tadalafil works by the same core mechanism: potent, selective PDE5 inhibition that elevates cGMP. Because the newly described cholesterol/NPC1 pathway depends on PDE5 blockade and the resulting cGMP rise (rather than a sildenafil-specific off-target effect), tadalafil is expected to engage it as well. The study itself refers more broadly to PDE5a inhibition and “Viagra-related drugs”/PDE5 inhibitors in the context of the findings and supporting clinical associations.

Supporting evidence from other research includes:Multiple preclinical studies in which both sildenafil and tadalafil reduced metastasis (e.g., perioperative models of melanoma and breast cancer lung metastases via effects on myeloid-derived suppressor cells/NK cells; other models of tumor growth, invasion, or metastasis).

Observational data linking PDE5 inhibitor use (sildenafil, tadalafil, vardenafil as a class) to lower metastasis risk and better outcomes in colorectal cancer and improved survival across various male-predominant cancers.

Additional work showing tadalafil activity against breast, head-and-neck, thyroid, melanoma, pancreatic, and other cancers, often via immune modulation (MDSC suppression, improved T-cell function) but also direct effects on proliferation/migration in some cell lines. Tadalafil has been tested in small clinical settings (e.g., melanoma, head-and-neck) with immunomodulatory signals.

Differences exist: tadalafil has a longer half-life (~17.5 hours vs. ~4 hours for sildenafil), different dosing patterns (often daily low-dose), and somewhat distinct selectivity/pharmacokinetics, which could influence tissue exposure, duration of cGMP elevation, or practical clinical use. Some older studies found variable direct antiproliferative potency across PDE5 inhibitors and cancer types. The specific NPC1/cholesterol trafficking mechanism is newly detailed mainly with sildenafil, so direct head-to-head confirmation for tadalafil on that pathway is still needed.Overall, the shared PDE5 target provides a strong mechanistic rationale for a comparable effect on the cholesterol-dependent metastatic pathway, and the broader literature on PDE5 inhibitors (including tadalafil) already supports anti-metastatic and anti-tumor potential through multiple routes. This remains preclinical/observational; it is not proven clinical therapy, and any use would require medical supervision due to side effects, interactions, and the need for proper trials.

I’m low dosing it, primarily because of evidence that it’s protective against heart disease, and it helps lower blood pressure, but this would be a nice side benefit.