PMD-026 reduced tumor growth in mice with triple negative breast cancer (TNBC), according to its developer, Phoenix Molecular Designs.
The therapy, which targets the RSK family of enzymes associated with cancer progression, was also safe, the company said.
TNBC is difficult to treat, not only because it behaves differently from patient to patient, but also because no therapies are effective against it.
PhoenixMD used genome screening to identify RSK, or p90 ribosomal S6 kinase, as a good target for TNBC therapies. The RSK family consists of four enzymes involved in cancer development. They are key regulators of cancer cell invasion and growth, but they are also associated with cancer cell drug resistance.
About 90 percent of TNBC cases are associated with abnormally high levels of two of the enzymes, RSK1 and RSK2. That suggests that the cancer cells rely on the enzymes’ activity for survival and proliferation. In fact, chemically inhibiting RSK2 in a lab killed TNBC cells and the cancer stem cells responsible for cancer recurring.
“The need for new targeted therapies to help patients suffering with TNBC is urgent, but unfortunately novel treatments are extremely scarce,” Sandra Dunn, chief executive officer of PhoenixMD, said in a press release. “We are addressing this unmet medical need through a novel, targeted approach by inhibiting critical kinases, such as RSK, known to be involved in the progression of numerous” cancers.
Researchers tested PMD-026 for 28 days in mice with drug-resistant TNBC. The drug lowered RKS’s activity by 70 percent, blocking cancer growth. There were no major adverse effects from the treatment, the team reported.
Researchers also compared PMD-026 with the standard of care treatment Adriamycin (doxorubicin). PMD-026 was as effective as Adriamycin at inhibiting TNBC growth and was safer, researchers found.
“Our recent favorable preclinical data on PMD-026, coupled with our robust intellectual property estate and leading research collaborations, give us greater confidence in our novel approach to treating cancer,” Dunn said. “We look forward to building upon these preclinical results and initiating first-in-man studies with PMD-026 in 2018.”
Because the cells implanted in the mice were resistant to drugs targeting the EGFR or mTOR proteins — such as Iressa (gefitinib) or Afinitor (everolimus) — the findings suggest that PMD-026 holds promise in treating patients with drug-resistant TNBC.
“The therapies being developed at PhoenixMD are designed to treat the most difficult cancer indications,” said Alan Lewis, CEO of the diabetes treatment developer Diavacs and chair of PhoenixMD’s Scientific Advisory Board. “They are also promising for strategic combinations with checkpoint inhibitors and/or standard of care therapies. I look forward to working with the established team at PhoenixMD to advance PMD-026 into the clinic.”
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