Patent classifications
A61K31/7034
Systems and methods for thrombosis prevention
The disclosure provides a composition for inhibiting thrombosis. The composition includes 5 to 25% by weight of Fish Oil, 15 to 55% by weight of Willow Bark Extract, and 0.2 to 5% by weight of Vitamin E.
Systems and methods for thrombosis prevention
The disclosure provides a composition for inhibiting thrombosis. The composition includes 5 to 25% by weight of Fish Oil, 15 to 55% by weight of Willow Bark Extract, and 0.2 to 5% by weight of Vitamin E.
Pharmaceutical composition for preventing or treating diabetes, containing zinc salt, cyclo-hispro and antidiabetic drug as active ingredients
The present invention relates to a pharmaceutical composition for preventing or treating diabetes, comprising, as active ingredients: (a) a zinc salt, comprising a zinc cation and anion, and cyclo-hispro, or a pharmaceutically acceptable salt thereof; and (b) an antidiabetic drug (particularly, an insulin sensitizer, an insulin sensitizer, a sodium-glucose co-transporter (a sodium-glucose co-transporter 2 (SGLT2) inhibitor), or a DPP-4 inhibitor).
Pharmaceutical composition for preventing or treating diabetes, containing zinc salt, cyclo-hispro and antidiabetic drug as active ingredients
The present invention relates to a pharmaceutical composition for preventing or treating diabetes, comprising, as active ingredients: (a) a zinc salt, comprising a zinc cation and anion, and cyclo-hispro, or a pharmaceutically acceptable salt thereof; and (b) an antidiabetic drug (particularly, an insulin sensitizer, an insulin sensitizer, a sodium-glucose co-transporter (a sodium-glucose co-transporter 2 (SGLT2) inhibitor), or a DPP-4 inhibitor).
Amylase inhibitor compounds, methods of their use and compositions thereof
There are provided compounds of Formula I: ##STR00001##
various compositions thereof and methods for their use in the inhibition of α-amylase.
Amylase inhibitor compounds, methods of their use and compositions thereof
There are provided compounds of Formula I: ##STR00001##
various compositions thereof and methods for their use in the inhibition of α-amylase.
Castration-resistant prostate cancer
This invention relates to inhibitors of UDP-glucose dehydrogenase, and more particularly to UDP-glucose dehydrogenase inhibitors that are useful in the treatment of prostate cancer. Methods of inhibiting UDP-glucose dehydrogenase and improving the efficacy of additional prostate cancer therapies are also provided.
Castration-resistant prostate cancer
This invention relates to inhibitors of UDP-glucose dehydrogenase, and more particularly to UDP-glucose dehydrogenase inhibitors that are useful in the treatment of prostate cancer. Methods of inhibiting UDP-glucose dehydrogenase and improving the efficacy of additional prostate cancer therapies are also provided.
Chimeric antigen receptor to which anti-cotinine antibody is linked, and use thereof
The present invention relates to chimeric antibody receptors with anti-cotinine antibodies linked, and use thereof. A T cell presenting the chimeric antibody receptor on the surface secretes interferon gamma specifically for a target molecule of a cotinine-conjugated binding molecule that is added together therewith and induces cell death of the cell expressing the target molecule by the T cell. On the contrary, by administering a cytotoxic agent conjugated with cotinine, cell death of the chimeric antigen receptor T cell is induced. Therefore, if necessary, a cytotoxic agent conjugated with cotinine can be administered to remove the chimeric antigen receptor T cells that have been already administered, thereby suppressing immune side effects due to hyperactivity of T cells. Thus, the chimeric antigen receptor to which the anti-cotinine antibody is linked can be effectively and safely used for the treatment of cancer.
Chimeric antigen receptor to which anti-cotinine antibody is linked, and use thereof
The present invention relates to chimeric antibody receptors with anti-cotinine antibodies linked, and use thereof. A T cell presenting the chimeric antibody receptor on the surface secretes interferon gamma specifically for a target molecule of a cotinine-conjugated binding molecule that is added together therewith and induces cell death of the cell expressing the target molecule by the T cell. On the contrary, by administering a cytotoxic agent conjugated with cotinine, cell death of the chimeric antigen receptor T cell is induced. Therefore, if necessary, a cytotoxic agent conjugated with cotinine can be administered to remove the chimeric antigen receptor T cells that have been already administered, thereby suppressing immune side effects due to hyperactivity of T cells. Thus, the chimeric antigen receptor to which the anti-cotinine antibody is linked can be effectively and safely used for the treatment of cancer.