tg02

SB1317 (TG02) is a potent inhibitor of cyclin dependant kinases (CDKs), Janus kinase 2 (JAK2), and Fms-like tyrosine kinase-3 (FLT3).

H 35-25 is a beta 2-antagonist.

Zotiraciclib (also known as TG02 and SB1317) is an innovative small-molecule compound with potent inhibitory effects on CDK, JAK2, and FLT3. By inhibiting cyclin-dependent kinase 9 (CDK9) and depleting Myc, it serves as a treatment for cancers that can penetrate the blood-brain barrier. Zotiraciclib is one of the numerous CDK inhibitors under investigation; other compounds targeting CDK9, utilized for treating acute myeloid leukemia, include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80% of glioblastomas exhibiting this characteristic.

(E/Z)-Zotiraciclib ((E/Z)-TG02) effectively inhibits CDK2, JAK2, and FLT3 with IC50s of 13 nM, 73 nM, and 56 nM, respectively.

SB1317 hydrochloride (1204918-72-8(free base)) (TG-02 hydrochloride) is an effective inhibitor of CDK2/JAK2/FLT3 (IC50: 13/73/56 nM).

(E/Z)-Zotiraciclib ((E/Z)-TG02) hydrochloride is a potent inhibitor of CDK2, JAK2, and FLT3.

(E/Z)-Zotiraciclib ((E/Z)-TG02) citrate is a potent inhibitor of CDK2, JAK2, and FLT3, making it suitable for use in cancer research.

Zotiraciclib, also known as TG02 and SB1317, is a novel small molecule potent CDK/JAK2/FLT3 inhibitor. Zotiraciclib may be useful for the treatment of cancer that crosses the blood brain barrier and acts by depleting Myc through the inhibition of cyclin-dependent kinase 9 (CDK9). It is one of a number of CDK inhibitors under investigation; others targeting CDK9 for the treatment of acute myeloid leukemia include alvocidib and atuveciclib. Myc overexpression is a known factor in many cancers, with 80 percent of glioblastomas characterized by this property.