NucleoBio’s investigative therapy Prostreat was seen to be better at preventing the growth and spread of metastatic castration-resistant prostate cancer than currently available hormone therapies, a mouse study showed.
The treatment was effective even in cells with a variant of the androgen receptor that renders them resistant to treatment, setting the basis for the development of Prostreat for the most aggressive form of prostate cancer.
The company is now planning to advance the therapy candidate into clinical trials later this year.
The findings were recently presented at the 25th Biennial Congress of the European Association for Cancer Research, held June 30-July 3 in Amsterdam.
The poster was titled, “Two novel synthetic analogues of miR-1207–3 p, NB5 and NB1207, target AR-V7 and c-MYC and demonstrate in vivo therapeutic efficacy in metastatic castrate-resistant prostate cancer (mCRPC).”
Mutations in a region of chromosome 8 are known to increase a patient’s susceptibility to prostate cancer. Researchers recently discovered that this happens because the mutations reduce the levels of a small RNA molecule, called miR-1207-3p, which leads to an increase in androgen receptor production.
Researchers set out to investigate whether miR-1207-3p could be used as a therapeutic approach for prostate cancer. The team was led by Olorunseun Ogunwobi, an MD and PhD, and investigator at Hunter College of The City University of New York (CUNY) and co-founder of NucleoBio.
Investigators first examined the levels of miR-1207-3p in prostate cancer tissue and compared them to those of healthy prostate tissue and benign prostatic hyperplasia (BPH) tissue samples.
They found that miR-1207-3p was significantly reduced in prostate cancer samples. And the more aggressive a cancer was, the lower the levels of this micro RNA.
In addition to being a possible biomarker for disease and aggressiveness, with the potential to identify aggressive cancers, researchers thought that miR-1207-3p, or compounds similar to miR-1207-3p, could be used to stop the disease.
They developed two compounds, NB1207 and NB5, which could mimic miR-1207-3p activity.
When tested in lab-grown cells, the compounds reduced c-MYC, a protein that supports cancer survival and progression. Importantly, when tested in cancer cells with a type of androgen receptor that is resistant to current treatments, AR-V7, the compounds significantly reduced the receptor levels.
This made the compounds effective at stopping the proliferation and killing cancer cells, which was not seen in commonly used treatments like Xtandi (enzalutamide), Zytiga (abiraterone), and Erleada (apalutamide).
In mice, NB1207 and NB5 significantly blocked tumor growth and stopped cancer cells from spreading, while Xtandi showed minimal impact. Zytiga and Erleada appeared to have no effect at all.
“We unveiled ineffectiveness in current therapies for this type of cancer and identified voids,” Charles Oyesile, an MD and PhD, co-founder and CEO of NucleoBio, said in a press release. “With the support of CUNY, we leveraged the latest advances in cancer research to create Prostreat, which outperformed current therapeutics in side-by-side laboratory tests.”
“This type of technology is relatively new, and to my knowledge, there is no other synthetic microRNA analog that is used in the treatment of prostate cancer,” Ogunwobi said.
Preliminary toxicology studies have shown that Prostreat has a good safety profile, with no toxic side effects reported in animals.
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