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U.S. pharmaceutical giants Gilead and Scholar Rock recently announced that they have entered into a strategic partnership to discover and develop highly specific conversion growth factor β (TGF beta) activation inhibitors for the treatment of fibrous diseases.
In this partnership, Gilead will have exclusive options to authorize the introduction of global rights to several candidate products from Scholar Rock's TGF beta program, including: inhibitors for high affinity and specific target latent TGF beta1 activation, selective targeting for inhibitors limited to extracellular substitut latent TGF beta1 activation, and a third TGF beta discovery project.
Scholar Rock will be responsible for antibody discovery and preclinical research until a drug candidate is nominated, after which Gilead will decide whether to exercise the option of the project, and if so, Gilead will be responsible for the project's preclinical research, clinical development and commercialization. Scholar Rock will retain certain TGF beta inhibitors found, developed and commercialized for use in oncology and cancer immunotherapy.
under the terms of the agreement, Scholar Rock will receive an advance of $80 million, including $50 million in cash and $30 million in acquisitions of the company's common stock. In addition, after completing a specific preclinical study, Scholar Rock will receive a one-time milestone payment of $25 million and will be eligible for a potential payment of $142.5 million, based on specific research, development, regulatory, and commercialization milestones in all three projects. Scholar Rock will also receive a 1-2-digit tiered royalties derived from future sales of its co-ed products.
fibrosis is a common characteristic of many diseases, which can lead to scarring of tissues and vital organs and is the leading cause of morbidity and death. The signal conduction path of TGF beta-mediated is considered to be the central regulator of fibrosis. The transfer of TGF beta signals to inhibitors found on the Scholar Rock proprietary platform has been shown in in-body and preclinical models to selectively prevent the activation of growth factors in fibrosis substates. By targeting disease microencases, these highly specific TGF beta activation inhibitors may provide new ways to inhibit pre-fibrosis signaling. (Bio Valley)