GPCR Therapeutics, Inc. announced it enters into an out-licensing agreement with Bridge Biotherapeutics (KQ288330) for the CXCR4-LPA1 inhibitor combination method of treatment. GPCR receives an upfront payment of KRW 2 billion (approx. USD 1.5 million), and a 50:50 profit-share on future commercialization, including sub-licenses.

In collaboration with Bridge Biotherapeutics, GPCR will pursue joint development and commercialization of the combination therapy. Conducting a multinational phase 2a clinical trial of BBT-877, an autotaxin inhibitor for the treatment of IPF, Bridge Biotherapeutics has been accelerating development of its proprietary IPF pipeline. Last September, GPCR published the paper on the direct interaction between two different GPCRs, CXCR4 and LPA1, in the peer-reviewed academic journal 'Cell Communication and Signaling'(1).

The target GPCRs are known to promote fibrotic diseases such as idiopathic pulmonary fibrosis (IPF). Through various in vitro experiments, the company found that the efficacy of LPA1 inhibition can be further maximized by inhibition of CXCR4, thereby securing a scientific basis that the CXCR4- LPA1 inhibitor combination may be necessary for full anti-fibrotic activity. Based on this finding, GPCR filed a provisional patent application on the CXCR4- Ltd. (KQ288330), for the CXCR4 and its inhibitory effect.

IPF is a progressive chronic lung condition that causes scarring (fibrosis) of a patients' lungs which makes breathing increasingly difficult as the lungs become stiffer and lose their elasticity. The lungs become less efficient at transferring oxygen so that when someone with IPF breathes in, the transfer of oxygen through airacs in their lungs and into their blood stream is impaired. Lung damage from IPF is irreversible, and there is currently no treatment that stops or reverses the scarring.

In the US there are around 495 cases per 100,000 people, with median survival estimated at 2-5 years from the time of diagnosis.