(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumor-associated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and
AMY-101 acetate (Cp40 acetate), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 acetate (Cp40 acetate) exhibits a favorable
AMY-101 acetate (Cp40 acetate), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 acetate (Cp40 acetate) exhibits a favorable
AMY-101 acetate (Cp40 acetate), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 acetate (Cp40 acetate) exhibits a favorable
AMY-101 acetate (Cp40 acetate), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 acetate (Cp40 acetate) exhibits a favorable
AMY-101 TFA (Cp40 TFA), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 (Cp40) exhibits a favorable anti-inflammatory activity in models
AMY-101 TFA (Cp40 TFA), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 (Cp40) exhibits a favorable anti-inflammatory activity in models
AMY-101 TFA (Cp40 TFA), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 (Cp40) exhibits a favorable anti-inflammatory activity in models
AMY-101 TFA (Cp40 TFA), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 (Cp40) exhibits a favorable anti-inflammatory activity in models
AMY-101 TFA (Cp40 TFA), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 (Cp40) exhibits a favorable anti-inflammatory activity in models
AMY-101 TFA (Cp40 TFA), a peptidic inhibitor of the central complement component C3 ( K D = 0.5 nM), inhibits naturally occurring periodontitis in non-human primates (NHPs). AMY-101 (Cp40) exhibits a favorable anti-inflammatory activity in models
ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the convertase-catalyzed activation of C5.Appearance:SolidBiological Activity:ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the
ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the convertase-catalyzed activation of C5.Appearance:SolidBiological Activity:ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the
ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the convertase-catalyzed activation of C5.Appearance:SolidBiological Activity:ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the
ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the convertase-catalyzed activation of C5.Appearance:SolidBiological Activity:ARC186, a aptamer, is highly potent complement inhibitors that function by blocking the