Williams Cancer Institute

VIAGRA AND ITS CONTRIBUTION IN THE TREATMENT AGAINST CANCER

Viagra, whose trade name (brand-name) is Sildenafil, is a medication whose first objective was to treat hypertension (blood pressure) and angina (chest pain); however, it also generated a curious side effect, men who had taken this medicine presented prolonged erections, but what is a side effect in one man is a happy night for another. This drug was patented in 1996 for the treatment of hypertension, in 1998 the FDA approved Sildenafil for erectile dysfunction and shortly after appeared two other similar drugs to treat erectile dysfunction—Cialis and Levitra.

However, the most common questions are: how can this medication help in the treatment of cancer? Is this medication safe for women? How does this medication work on our immune system? does this drug provide a boost to fight cancer?

Viagra, Cialis, and Levitra belong to a class of PDE-5 drugs. This means that one of its “side effects” is the reduction of MDSCs (Myeloid Derived Suppressor Cells), an important aspect for the immune system to attack tumors.

MDSCs are similar to regulatory T-cells MDSCs also interfere with antitumor immunity, and they do so by using L-arginine metabolism to suppress immunity.

Arginine is a critical amino acid for a healthy immune system as it is needed to activate T cells, but when cancer is present, tumors and regulatory immune cells produce an enzyme called Arginase 1 that breaks down arginine in the microenvironment of the body tumor.

Nevertheless, phosphodiesterase-5 inhibitors control this process, also known as PDE-5. PDE-5 inhibitors reduce myeloid-derived suppressor cells and suppress arginase production, that means that tumors have one less ally in their quest to grow and reproduce.

Moreover, the role of MDSCs in the immune response is an important topic in cancer research nowadays. Although there are not treatments available specifically to control them. Currently, the best source of PDE-5 and Arginase 1 inhibitors available are the popular erectile dysfunction drugs Viagra, Cialis, and Levitra.

Likewise, women can safely take these medications. It has not yet been proven that taking these medications increases sexual desire, although cases have been reported in which it seems to happen, but, just as the aforementioned medications, they stimulate blood flow to the penis, they can stimulate blood flow to the genitals of the woman which can increase sensitivity to stimulation. This is not such a bad side effect when the goal is to increase the stimulation of the immune response for a woman who is fighting cancer.

These medications need to be taken under the supervision of a doctor. Drugs such as Viagra, Cialis and Levitra can cause a significant drop in blood pressure. Patients with low blood pressure would not be able to use them.

Nor can we think that Viagra was only good for treating erectile dysfunction, now it is also used as a cancer treatment since it increases the stimulation of the immune response since it has been discovered that phosphodiesterase type 5, or inhibitors of PDE5, can help shrink cancerous tumors, thus becoming an unexpected anticancer drug.

Cancer also tends to get worse faster; this is because the microenvironment (the area directly around the tumor) contains molecules and blood vessels that have become contaminated, these form a protective area around the tumor, making it resistant to treatment.

Due to Viagra and other PDE5 inhibitors appear to make CAFs more sensitive to immunotherapy treatment, this drug could be a reliable and effective anticancer drug that lessens the morbid outcomes seen in earlier studies, therefore, it is known that the effectiveness offered by Viagra as a drug against cancer could open new doors for research and treatment.

References:  Joshua Hawkins, 2022, 10th October, Doctors may have found a secret weapon to fight cancer: Viagra, https://bgr.com/science/doctors-may-have-found-a-secret-weapon-to-fight-cancer-viagra/

Williams, J. (2019, 15th October) The Immunotherapy Revolution. (pp. 108-110)

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