(Z)-Leukadherin-1 (Synonyms: ADH-503 free base) |
Katalog-Nr.GC38880 |
(Z)-Leukadherin-1 (ADH-503 freie Base) ist ein oral aktiver und allosterischer CD11b-Agonist. (Z)-Leukadherin-1 fÜhrt zur Repolarisation tumorassoziierter Makrophagen, zur Verringerung der Anzahl tumorinfiltrierender immunsuppressiver myeloider Zellen und verstÄrkt die Antworten dendritischer Zellen.
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Cas No.: 2055362-72-4
Sample solution is provided at 25 µL, 10mM.
(Z)-Leukadherin-1 (ADH-503 free base) is an orally active and allosteric CD11b agonist. (Z)-Leukadherin-1 leads to the repolarization of tumorassociated macrophages, reduction in the number of tumor-infiltrating immunosuppressive myeloid cells, and enhances dendritic cell responses[1].
(Z)-Leukadherin-1 (ADH-503 free base; 4 μM; 8 days) reduces the numbers of total tumor-infiltrating CD11b+ cells and subsets of CD11b+ monocytes, granulocytes, eosinophils, and macrophages[1].
(Z)-Leukadherin-1 (ADH-503 free base; oral gavage; 30, 60, or 120 mg/kg; twice a day for 60 days) delayes tumor progression, leading to a significantly decreased tumor burden in time-point analysis and improved overall survival[1]. (Z)-Leukadherin-1 (oral gavage; 30, 100 mg/kg; twice a day; on days 1 and 5) has the mean half-life of 4.68 and 3.95 hours, a maximum concentration of 1716 and 2594 ng/ml and AUC0-t in the plasma of 6950 and 13962 ng.h/ml at 30 and 100 mg/kg dosing, respectively[1]. Animal Model: KPC mice [p48-CRE/Lox-stop-Lox(LSL)-KrasG12D/p53flox/flox][1]
[1]. Panni RZ, et al. Agonism of CD11b reprograms innate immunity to sensitize pancreatic cancer to immunotherapies. Sci Transl Med. 2019 Jul 3;11(499).
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