BEVERLY HILLS, Calif., Oct. 7, 2015 /PRNewswire/ -- Rich Pharmaceuticals, Inc. (OTCPK: RCHA) ("Rich" or the "Company") announced today it has entered into an agreement with Theradex Systems, Inc. ("Theradex"), a leading global contract research organization ("CRO") with extensive expertise in oncology clinical development. Through this new partnership, Theradex will lead the Company in finalizing the Investigational New Drug Application (IND #124642) with the U.S. FDA for Rich's lead drug RP-323 in patients with AML.
"We selected Theradex to take over CRO duties for RP-323 development in AML because of Theradex's proven excellence in oncology clinical research and their reliability working in conjunction with the FDA in drug development and the FDA approval process." said Ben Chang, CEO of Rich. "After our most recent discussion with the FDA, we believe we now have clear direction for finalizing the IND, and we are optimistic that we will be able to move into clinical trials in 2016. The expansion of our team, through our collaboration with Theradex, should allow us to advance the RP-323 program as efficiently and quickly as possible and is expected to help Rich take the last step needed to fulfill the FDA's final requirements."
Rich Pharmaceuticals is a clinical-stage biotechnology company focused on developing innovative therapies in oncology, with initial concentration in treating AML, Myelodysplastic Syndromes (MDS) and Hodgkin's Lymphoma. The lead "platform drug" (RP-323) is a phorbol ester, which induces differentiation and/or apoptosis in multiple cell lines and primary cells, activates protein kinase C (PKC), and modulates the activity of multiple downstream cell signaling pathways, including mitogen-activated protein kinase (MAPK) pathways. TPA induces PKC to produce NF kappa, which produces NF kappa B that has the ability to regulate cellular responses by entering into the nucleus of cell. NF kappa B binds to DNA and changes the nature of the cell and (1) induces differentiation; (2) induces proliferation; (3) cytokine induction; (4) and/or apoptosis.
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