3AC

A cell-permeable steroidal compound that selectively inhibits SHIP1-, but not SHIP2-, catalyzed PI(3,4,5)P3-to-PI(3,4)P2 dephosphorylation (IC₅₀ = 10 µM vs. >1 mM, respectively), while exhibiting little activity against the PTEN-catalyzed PI(3,4,5)P3-to-PI(4,5)P2 conversion (IC₅₀ >1 mM). 3AC in vivo treatment (2.292 umol/200 µl/mouse/daily i.p. for 7 d) is reported to boost both peripheral blood granulocyte production (by 4- to 5-fold) and the GVHD- (graft-versus-host disease) suppressing Mac1⁺Gr1⁺ MIR (myeloid immunoregulatory) cell population in lymphoid tissues (by 5.55- and 11.53-fold in spleen and lymph nodes, respectively), resulting in an impaired splenocyte allogeneic T cell response in MLR (mixed-leukocyte/lymphocyte reaction) assays (by ≥95%). Similarly, 3AC-treated (9.4 µM; 24 h) primary human PBMCs greatly lose their ability in priming allogeneic T cell response in MLR assays (by 74.5%). In addition, a faster blood cell recovery is also observed in mice receiving 3AC (2.292 umol/200 µl/mouse/daily i.p. for 7 d) after sub-lethal irradiation (550 Rads). Selectively inhibits the growth and survival of SHIP1-dependent human KG-1 and murine C1498 myelogenous leukemia lines (IC₅₀ = 11.5 µM), but not the SHIP1-negative human CML K562 and osteosarcoma MG63 lines. SHIP2 Inhibitor, AS1938909 is also available (Cat. No. 565840).

Packaged under inert gas

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

Brooks, R., et al. 2010. J. Immunol.184, 3582.

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Toxicity: Standard Handling (A)