PSGL-1, as a new target of global innovative immunotherapy, can cause macrophage reprogramming and stimulate synergistic antitumor response.

 

 

 

Sansheng Guojian Pharmaceutical (Shanghai) Co., Ltd., a subsidiary of Sansheng Pharmaceutical , will be responsible for the development and commercialization of vtx-0811 in mainland China, Taiwan, Hong Kong and Macau ("the region").

 

 

 

By targeting PSGL-1, a highly expressed adhesion molecule on tumor associated macrophages, vtx-0811 reprogrammes macrophages into a pro-inflammatory state, activates T cells and attracts other immune cells to produce powerful antitumor effects. In response to PD-1 and unresponsive tumors, Verseau's PSGL-1 antibody showed a stronger inflammatory response than the current immunotherapy.

 

 

 

PSGL-1 is the first target in the Verseau macrophage checkpoint regulator pipeline to enter the development stage. Verseau's macrophage checkpoint regulator reprogrammes macrophages to make them more inflammatory or tolerable depending on the condition of the disease.

 

 

 

Under the terms of the agreement, Sansheng pharmaceutical will obtain an exclusive license in the region to develop and commercialize a series of macrophage checkpoint regulatory antibodies for all human tumor indications.

 

 

 

Verseau reserves the global interest in all macrophage checkpoint conditioning projects outside Greater China.

 

 

 

Verseau will be responsible for the early detection and optimization of macrophage checkpoint modulator antibody products. Sansheng pharmaceutical will carry out preclinical and clinical development, product production, registration and commercialization of new drugs (http://www.chemdrug.com/) at macrophage checkpoints in the region.

 

 

 

Verseau and Sansheng will be eligible for certain milestone payments and royalties for product sales in the region and globally. The first joint development project selected under the partnership will result in a milestone payment for Verseau, the amount of which is not disclosed.