NLG802 is an orally bioavailable prodrug of indoximod, a methylated tryptophan, with immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, the indoximod prodrug NLG802 is converted to indoximod. Indoximod targets, binds to and inhibits the enzyme indoleamine 2,3-dioxygenase (IDO; IDO1), which converts the essential amino acid tryptophan into the immunosuppressive metabolite kynurenine. By increasing tryptophan levels and decreasing kynurenine levels, indoximod restores and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T lymphocytes, and causes a reduction in tumor-associated regulatory T cells (Tregs).
NLG802 is an orally bioavailable prodrug of indoximod, a methylated tryptophan, with immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, the indoximod prodrug NLG802 is converted to indoximod. Indoximod targets, binds to and inhibits the enzyme indoleamine 2,3-dioxygenase (IDO; IDO1), which converts the essential amino acid tryptophan into the immunosuppressive metabolite kynurenine. By increasing tryptophan levels and decreasing kynurenine levels, indoximod restores and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T lymphocytes, and causes a reduction in tumor-associated regulatory T cells (Tregs).
NLG802 is an orally bioavailable prodrug of indoximod, a methylated tryptophan, with immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, the indoximod prodrug NLG802 is converted to indoximod. Indoximod targets, binds to and inhibits the enzyme indoleamine 2,3-dioxygenase (IDO; IDO1), which converts the essential amino acid tryptophan into the immunosuppressive metabolite kynurenine. By increasing tryptophan levels and decreasing kynurenine levels, indoximod restores and promotes the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T lymphocytes, and causes a reduction in tumor-associated regulatory T cells (Tregs).
评论内容