Researchers from the University of Pittsburgh have demonstrated that a soluble guanylate cyclase activator has the potential to treat age related prostatic hyperplasia and prostate cancer.
Description
In the USA alone there are over a quarter of a million new cases of prostate cancer every year, accounting for nearly 35,000 deaths annually, over 10% of all cancer deaths in men. Treatment options for the more severe patient cases can include surgery, radiotherapy, and androgen deprivation therapy. This approach can destroy most cancerous cells, but surviving cells can become senescent and resistant to treatment, increasing the risk of reoccurrence. The novel approach described here can target these senescent cells, inducing apoptosis with the potential to improve patient outcomes.
Applications
• Benign prostatic hyperplasia (BPH)
• Prostate Cancer
Advantages
With a large mortality rate, treatment options for prostate cancer remain an unmet clinical need. A challenge is the senescent cells resistant to treatment which can remain after irradiation and chemotherapy. Senescent cells inhibit mitophagy, leading to accumulation of damaged mitochondria, in turn causing inflammation and cytokine secretion. This can promote tumor re-emergence through increased expression of pro-growth Bc1-2 which inhibits pro-apoptotic BAX.
Senescent cells can be managed in two ways, either through induced mitophagy and recovery from senescence to reduce cytokine release or through inducing apoptosis, completely clearing out the senescent cells. Research from the University of Pittsburgh has demonstrated better results are achieved with apoptosis. Based on the development of androgen resistance being linked to overexpression of the sGC?1 subunit in prostate cancer, a soluble guanylate cyclase (sGC) activator has the potential to target androgen resistant cells and induce apoptosis overcoming many of the challenges presented with existing treatment regimens.
Invention Readiness
Cinaciguat, an sGC activator, has been shown in mice models to reverse benign prostatic hyperplasia in aged mice by decreasing the Bc1-2/BAX ratio. Additional research has suggested a similar mechanism of action in irradiated mouse prostate tumors preventing tumor re-emergence and promoting apoptosis and clearance of senescent cells.
IP Status
https://patents.google.com/patent/US20240335408A1
