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Imatinib

MCE China：Imatinib

Brand：MedChemExpress (MCE)

Cat. No.HY-15463

CAS：152459-95-5

Synonyms：STI571; CGP-57148B

Purity：99.95%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 1 year -20°C 6 months

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Imatinib (STI571) is an orally bioavailable tyrosine kinases inhibitor that selectively inhibits BCR/ABL, v-Abl, PDGFR and c-kit kinase activity. Imatinib (STI571) works by binding close to the ATP binding site, locking it in a closed or self-inhibited conformation, therefore inhibiting the enzyme activity of the protein semicompetitively. Imatinib also is an inhibitor of SARS-CoV and MERS-CoV.

In Vitro：Imatinib (STI571) inhibits c-Kit autophosphorylation, activation of MAPK, and activation of Akt without altering total protein levels of c-kit, MAPK, or Akt. The concentration that produces 50% inhibition for these effects is approximately 100 nM[1]. Imatinib (STI571) is very effective (in vitro IC50 of 25 nM) against the chronic myeloid leukemia-causing kinase Bcr-Abl. Imatinib also efficiently inhibits Kit (in vitro IC50, 410 nM) and PDGFR (in vitro IC50, 380 nM)[2]. Imatinib (STI571) is a multi-target inhibitor of v-Abl, c-Kit and inhibits Bcr/Abl, v-Abl, Tel/Abl, the native PDGFβ receptor, and c-Kit, but it does not inhibit Src family kinases, c-Fms, Flt3, the EGFR or multiple other tyrosine kinases. Imatinib inhibits tyrosine phosphorylation and cell growth of Ba/F3 cells expressing Bcr/Abl, Tel/Abl, Tel/PDGFβR, and Tel/Arg with an IC50 of approximately 0.5 μM in each case, but it has no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by Tel/JAK2[4]. The IC50s of Imatinib(STI571) is a multi-target inhibitor of v-Abl, c-Kit and on BON-1 and H727 cells after exposure for 48 h are 32.4 and 32.8 μM, respectively[6].

In Vivo：In the phosphorothioate antisense oligodeoxynucleotides (PS-ASODN) group, tumor growth is inhibited by 59.437%, which is markedly higher than in the Imatinib (STI571) is a multi-target inhibitor of v-Abl, c-Kit and group (11.071%) and liposome negative control group (2.759%). Telomerase activity is significantly lower (Pliposome negative control group (2.013±0.273), and saline group (2.004±0.163)[7]. Imatinib (25 mg/kg/day, p.o.) suppresses the growth of endometriotic tissue and reduces the number of ovarian follicles in a rat model. Imatinib effectively treats experimental endometriosis by its inhibitor effects on angiogenesis and cell proliferation[8].

Animal Administration：Mice[6] The 40 tumor-bearing SCID mice are randomly divided into four groups (10 mice per group): the PS-ASODN group (5 μM, each mouse receives 0.2 mL by intratumor injection once daily); Imatinib group (0.1 mg/g body weight); liposome negative control group (0.01 mL/g); and saline group (0.01 mL/g). The mice in each group receive the relevant treatment by intra-tumor injection once daily from day 7 to day 28 after implantation. After 28 d, the mice are sacrificed, and tumor weight and longest and shortest diameters are measured by electronic scale and vernier caliper, respectively. Inhibition of tumor growth is calculated. Rats[7] Adult female Wistar-Albino rats (220-240 g) are used. Twenty-one days after the first surgical procedure, the rats undergo a second laparotomy to evaluate the occurrence of endometriosis. Twenty-four rats have visually confirmed endometriotic implants and are randomized into three groups to receive Imatinib (25 mg/kg/day, p.o.), Anastrozole (0.004 mg/day, p.o.), or normal saline (0.1 mL, i.p.) for 14 days.

Cell Assay：BON-1 cells (7,500 per well) and NCI-H727 cells (5,000 per well) are seeded into flat-bottomed 96-well plates in triplicate and allowed to adhere overnight in 10% fetal bovine serum-supplemented DMEM or RPMI 1640 complete medium, respectively; the medium is then exchanged for serum-free medium (negative control) or serum-free medium containing serial dilutions of Imatinib. After 48 h (control cultures do not reach confluence), the number of metabolically active cells is determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and absorbance is measured in a Packard Spectra microplate reader at 540 nm. Growth inhibition is calculated. Experiments are done in triplicates[4].

IC50 & Target：BCR/ABL, v-Abl, PDGFR, c-kit[1][2][4] Cellular Effect Cell Line Type Value Description References

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References：

[1]. Heinrich MC, et al. Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood. 2000 Aug 1;96(3):925-32.  [Content Brief]

[2]. Guida T, et al. Sorafenib inhibits imatinib-resistant KIT and platelet-derived growth factor receptor beta gatekeeper mutants. Clin Cancer Res. 2007 Jun 1;13(11):3363-9.  [Content Brief]

[3]. Iqbal N, et al. Imatinib: a breakthrough of targeted therapy in cancer. Chemother Res Pract. 2014;2014:357027.  [Content Brief]

[4]. Okuda K, et al. ARG tyrosine kinase activity is inhibited by STI571.Blood. 2001 Apr 15;97(8):2440-8  [Content Brief]

[5]. Jeanne M Sisk, et al. Coronavirus S Protein-Induced Fusion Is Blocked Prior to Hemifusion by Abl Kinase Inhibitors. J Gen Virol. 2018 May;99(5):619-630.  [Content Brief]

[6]. Yao JC, et al. Clinical and in vitro studies of imatinib in advanced carcinoid tumors. Clin Cancer Res. 2007 Jan 1;13(1):234-40.  [Content Brief]

[7]. Sun XC, et al. Depletion of telomerase RNA inhibits growth of gastrointestinal tumors transplanted in mice. World J Gastroenterol. 2013 Apr 21;19(15):2340-7.  [Content Brief]

[8]. Yildiz C, et al. Effect of imatinib on growth of experimental endometriosis in rats. Eur J Obstet Gynecol Reprod Biol. 2016 Feb;197:159-63.  [Content Brief]

[9]. Coleman CM, et al, Frieman MB. Abelson Kinase Inhibitors Are Potent Inhibitors of Severe Acute Respiratory Syndrome Coronavirus and Middle East Respiratory Syndrome Coronavirus Fusion. J Virol. 2016;90(19):8924‐8933. Published 2016 Sep 12.  [Content Brief]