CX-4945 sodium salt

Research use only, not for human use.

A potent, selective, orally bioavailable, ATP-competitive inhibitor of protein kinase CK2 with Ki of 0.38 nM, CK2α IC50 of 1 nM.

A potent, selective, orally bioavailable, ATP-competitive inhibitor of protein kinase CK2 with Ki of 0.38 nM, CK2α IC50 of 1 nM; displays good selectivity profile against a panel of 238 kinases; attenuates PI3K/Akt signaling, blocks CK2-dependent HIF-1α transcription, caused cell cycle arrest and selectively induces apoptosis in cancer cells relative to normal cells; exhibits antitumor efficacy in murine xenograft models.Blood Cancer Phase 2 Clinical(In Vitro):Silmitasertib (CX-4945) causes cell-cycle arrest and selectively induces apoptosis in cancer cells relative to normal cells, attenuates PI3K/Akt signalingand, and the antiproliferative activity of Silmitasertib (CX-4945) is correlated with expression levels of the CK2α catalytic subunit, Attenuation of PI3K/Akt signaling. Silmitasertib (CX-4945) with PS-341 treatment prevents leukemic cells from engaging a functional UPR in order to buffer the PS-341-mediated proteotoxic stress in ER lumen, and decreases pro-survival ER chaperon BIP/Grp78 expression. Silmitasertib (CX-4945) induces cytotoxicity and apoptosis, and exerts anti-proliferative effects in hematological tumors by downregulating CK2 expression and suppressing activation of CK2-mediated PI3K/Akt/mTOR signaling pathways.(In Vivo):Silmitasertib (CX-4945) (25 or 75 mg/kg, p.o.) is well tolerated and demonstrated robust antitumor activity with concomitant reductions of the mechanism-based biomarker phospho-p21 (T145) in murine xenograft models.

Silmitasertib (CX-4945) causes cell-cycle arrest and selectively induces apoptosis in cancer cells relative to normal cells, attenuates PI3K/Akt signalingand, and the antiproliferative activity of Silmitasertib (CX-4945) is correlated with expression levels of the CK2α catalytic subunit, Attenuation of PI3K/Akt signaling. Silmitasertib (CX-4945) with PS-341 treatment prevents leukemic cells from engaging a functional UPR in order to buffer the PS-341-mediated proteotoxic stress in ER lumen, and decreases pro-survival ER chaperon BIP/Grp78 expression. Silmitasertib (CX-4945) induces cytotoxicity and apoptosis, and exerts anti-proliferative effects in hematological tumors by downregulating CK2 expression and suppressing activation of CK2-mediated PI3K/Akt/mTOR signaling pathways.

Silmitasertib (CX-4945) (25 or 75 mg/kg, p.o.) is well tolerated and demonstrated robust antitumor activity with concomitant reductions of the mechanism-based biomarker phospho-p21 (T145) in murine xenograft models.

Silmitasertib sodium salt

Metabolic Enzyme/Protease

Casein Kinase

Casein Kinase

Cancer

Blood cancer

1309357-15-0

371.7523

C19H11ClN3NaO2

>98% (HPLC)

10 mM in DMSO

O=C(C1=CC=C2C(N=C(NC3=CC=CC(Cl)=C3)C4=C2C=NC=C4)=C1)[O-].[Na+]

Benzo[c]-2,6-naphthyridine-8-carboxylic acid, 5-[(3-chlorophenyl)amino]-, sodium salt (1:1)

(-20℃)

With Ice Pack

≥ 2 years