JAK1-IN-4 is a potent and selective JAK1 inhibitor, with IC50s of 85 nM, 12.8 μM and >30 μM for JAK1, JAK2, and JAK3, respectively. JAK1-IN-4 inhibits STAT3 phosphorylation in NCI-H 1975 cells (IC50, 227 nM)[1].
IC50 & Target[1]
JAK1
85 nM (IC50)
JAK2
12.8 μM (IC50)
分子量
521.59
Formula
C26H32FN9O2
CAS 号
2091134-35-7
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Annika Birgitta Margareta ÅSTRAND, et al. Compounds and methods for inhibiting jak.
SJ10542 is a potent and selective JAK2/3 directing phenyl glutarimide (PG)-PROTAC with DC50s of 14, 11, and 24 nM for JAK2, JAK3, and JAK2-fusion ALL, respectively. SJ10542 utilizes a PG ligand as the cereblon (CRBN) recruiter[1].
IC50 & Target[1]
JAK2
14 nM (DC50)
JAK3
11 nM (DC50)
Cereblon
JAK2-fusion ALL
24 nM (DC50)
分子量
818.95
Formula
C41H46N12O5S
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Lisa J.Alcock,et al. Development of Potent and Selective Janus Kinase 2/3 Directing PG-PROTACs.ACS Med.Chem.Lett.2022,13,3,475-482.
XL019 is a potent, orally active, and selective JAK2 inhibitor, with IC50s of 2.2, 134.3, and 214.2 nM for JAK2, JAK1 and JAK3, respectively. XL019 shows 50-fold or greater selectivity for JAK2, versus a panel of over 100 serine/threonine and tyrosine kinases, including other members of the JAK family. XL019 potently inhibits STAT3 and STAT5 phosphorylation in cells harboring either JAK2V617F or wild-type JAK2[1][2].
IC50 & Target[1]
JAK2
2.2 nM (IC50)
JAK3
214.2 nM (IC50)
体内研究 (In Vivo)
XL019 (100-300 mg/kg; p.o.; twice daily for 14 days) inhibits HEL.92.1.7 xenograft tumor growth[1]. XL019 (10 mg/kg) treatment shows that the Cmax, t1/2 and Vd were 5.24 μM, 1.94 hours, 5.319 L/kg, respectively[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female nude mice (HEL.92.1.7 xenograft tumors)[1]
Dosage:
100, 200, 300 mg/kg
Administration:
p.o.; twice daily for 14 days
Result:
Inhibition of HEL.92.1.7 xenograft tumor growth.
Animal Model:
Mouse[1]
Dosage:
10 mg/kg
Administration:
p.o.(Pharmacokinetic Analysis)
Result:
The Cmax, t1/2 and Vd were 5.24 μM, 1.94 hours, and 5.319 L/kg, respectively.
Clinical Trial
分子量
444.53
Formula
C25H28N6O2
CAS 号
945755-56-6
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Forsyth T, et al. SAR and in vivo evaluation of 4-aryl-2-aminoalkylpyrimidines as potent and selective Janus kinase 2 (JAK2) inhibitors. Bioorg Med Chem Lett. 2012 Dec 15;22(24):7653-8.
[1]. Jin Li, et al. Composés d’imidazo[1,2-a]pyridin-2-ylamine substitués, compositions pharmaceutiques et leurs méthodes d’utilisation. Patent WO2016119700A1.
Itacitinib (INCB039110) is an orally active and selective inhibitor of JAK1 with an IC50 of 2 nM for human JAK1. Itacitinib shows >20-fold selectivity for JAK1 over JAK2 and >100-fold over JAK3 and TYK2; Itacitinib is used in the research of myelofibrosis[1][2].
IC50 & Target[1]
JAK1
体外研究 (In Vitro)
Itacitinib (INCB039110) is a potent and selective inhibitor of JAK1, with >20-fold selectivity for JAK1 over JAK2 and >100-fold over JAK3 and TYK2. Itacitinib is used in the research of myelofibrosis[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
553.51
Formula
C26H23F4N9O
CAS 号
1334298-90-6
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Mascarenhas JO, et al. Primary analysis of a phase II open-label trial of INCB039110, a selective JAK1 inhibitor, in patients with myelofibrosis. Haematologica. 2017 Feb;102(2):327-335.
[2]. Alain Lescoat, et al. Combined Anti-Fibrotic and Anti-Inflammatory Properties of JAK-inhibitors on Macrophages in Vitro and in Vivo: Perspectives for Scleroderma-Associated Interstitial Lung Disease. Biochem Pharmacol. 2020 Jun 17;114103.
JAK1/TYK2-IN-1 is a dual inhibitor of TYK2 and JAK1 (IC50 = 29 and 41 nM respectively).
分子量
407.39
Formula
C18H20F3N7O
CAS 号
1883300-48-8
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Fensome A, et al. Design and optimization of a series of 4-(3-azabicyclo[3.1.0]hexan-3-yl)pyrimidin-2-amines: Dual inhibitors of TYK2 and JAK1. Bioorg Med Chem. 2020 May 15;28(10):115481.
JAK/HDAC-IN-1 is a potent JAK2/HDAC dual inhibitor, exhibits antiproliferative and proapoptotic activities in several hematological cell lines. JAK/HDAC-IN-1 shows IC50s of 4 and 2 nM for JAK2 and HDAC, respectively[1].
IC50 & Target[1]
JAK2
4 nM (IC50)
JAK1
4.8 nM (IC50)
JAK3
7.4 nM (IC50)
Tyk2
49 nM (IC50)
HDAC
2 nM (IC50)
HDAC2
14 nM (IC50)
HDAC6
120 nM (IC50)
HDAC8
2470 nM (IC50)
体外研究 (In Vitro)
JAK/HDAC-IN-1 (Compound 8m) exhibits IC50s of 4.8, 7.4 and 49 nM for JAK1, JAK3 and TYK2, and 14, 120, 2470 nM for HDAC2, HDAC6 and HDAC8, respectively[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
450.32
Formula
C19H21Cl2N7O2
CAS 号
2284621-75-4
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Liang X, et al. Discovery of Novel Janus Kinase (JAK) and Histone Deacetylase (HDAC) Dual Inhibitors for the Treatment of Hematological Malignancies. J Med Chem. 2019 Apr 25;62(8):3898-3923.
JAK2-IN-7 is a selective JAK2 inhibitor with IC50s of 3, 11.7, and 41 nM for JAK2, SET-2, and Ba/F3V617F cells, respectively. JAK2-IN-7 possesses >14-fold selectivity over JAK1, JAK3, FLT3. JAK2-IN-7 stimulates cell cycle arrest in the G0/G1 phase and induces tumor cellapoptosis. Antitumor activities[1].
IC50 & Target[1]
JAK1
42 nM (IC50)
JAK2
3 nM (IC50)
JAK3
94 nM (IC50)
Tyk2
75 nM (IC50)
FLT3
62 nM (IC50)
体外研究 (In Vitro)
JAK2-IN-7 (compound 13ac) (0-1000 nM; 2 hours) inhibits JAK2 and STAT5 phosphorylation in a dose-dependent manner in SET-2 and Ba/F3-JAK2V617F cells[1]. JAK2-IN-7 (10-160 nM; 24 hours) induces cell arrest in the G0/G1 phase[1]. JAK2-IN-7 (0.05-1.6 μM; 2 hours) induces apoptosis in SET-2 cells[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Cycle Analysis[1]
Cell Line:
SET-2 cells
Concentration:
10-160 nM
Incubation Time:
24 hours
Result:
Induced cell arrest in the G0/G1 phase in a concentration-dependent manner.
Apoptosis Analysis[1]
Cell Line:
SET-2 cells
Concentration:
0.05-1.6 μM
Incubation Time:
2 hours
Result:
Induced apoptosis in SET-2 cells.
体内研究 (In Vivo)
JAK2-IN-7 (15-60 mg/kg; p.o.; daily for 16 days) shows potent in vivo antitumor efficacy with 82.3% tumor growth inhibition in the SET-2 xenograft model[1]. JAK2-IN-7 (30-60 mg/kg; p.o.; q.d. for 16 day) significantly ameliorates the disease symptoms in a Ba/F3-JAK2V617F allograft model, with 77.1% normalization of spleen weight, which was more potent than Ruxolitinib[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
[1]. Yang T, et al. N-(Pyrimidin-2-yl)-1,2,3,4-tetrahydroisoquinolin-6-amine Derivatives as Selective Janus Kinase 2 Inhibitors for the Treatment of Myeloproliferative Neoplasms [published online ahead of print, 2020 Nov 30]. J Med Chem. 2020;10.1021/acs.jmedchem.0c01488.
JAK2/FLT3-IN-1 is a potent and orally active dual JAK2/FLT3 inhibitor with IC50 values of 0.7 nM, 4 nM, 26 nM and 39 nM for JAK2, FLT3, JAK1 and JAK3, respectively. JAK2/FLT3-IN-1 has anti-cancer activity[1].
IC50 & Target[1]
JAK2
0.7 nM (IC50)
FLT3
4 nM (IC50)
JAK1
26 nM (IC50)
JAK3
39 nM (IC50)
体外研究 (In Vitro)
JAK2/FLT3-IN-1 (0.008-1 μM; for 2 hours) down-regulates p-FLT3 in a dose-dependent manner[1]. JAK2/FLT3-IN-1 (5-100 nM; for 2 hours) has a dose-dependent effect on the induction of apoptosis in the MV4-11 cells[1]. JAK2/FLT3-IN-1 (5-100 nM; for 2 hours) strongly induces cell cycle arrest with a G1/G0 percentage of 85% at 100 nM in the MV4-11 cells[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[1]
Cell Line:
MV4-11 and SET-2 cells
Concentration:
0.008, 0.04, 0.2, 1 μM
Incubation Time:
For 2 hours
Result:
Down-regulated p-FLT3 in a dose-dependent manner from 0.008 to 1 μM.
Apoptosis Analysis[1]
Cell Line:
MV4-11 cells
Concentration:
5, 10, 50, 100 nM
Incubation Time:
For 2 hours
Result:
Had a dose-dependent effect on the induction of apoptosis in the MV4-11 cells.
Cell Cycle Analysis[1]
Cell Line:
MV4-11 cells
Concentration:
5, 10, 50, 100 nM
Incubation Time:
For 2 hours
Result:
Induced cell cycle arrest with a G1/G0 percentage of 85% at 100 nM.
体内研究 (In Vivo)
JAK2/FLT3-IN-1 (30 and 60 mg/kg/day; p.o.; for 14 days) exhibits significant antitumor effects[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
NOD/SCID mouse models[1]
Dosage:
30 and 60 mg/kg
Administration:
Oral administration; daily; for 14 days
Result:
Exhibited significant antitumor effects. The tumor growth inhibitory rates (TGI) were respective 58% and 93% in the MV4-11-bearing mice model.
分子量
467.58
Formula
C25H34FN7O
CAS 号
2387765-27-5
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
溶解性数据
In Vitro:
DMSO : 20.83 mg/mL (44.55 mM; ultrasonic and warming and heat to 60°C)
配制储备液
浓度溶剂体积质量
1 mg
5 mg
10 mg
1 mM
2.1387 mL
10.6934 mL
21.3867 mL
5 mM
0.4277 mL
2.1387 mL
4.2773 mL
10 mM
0.2139 mL
1.0693 mL
2.1387 mL
In Vivo:
请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
*以上所有助溶剂都可在 Shanghai Jinpan Biotech Co Ltd 网站选购。
参考文献
[1]. Yang T, et al. Discovery of Potent and Orally Effective Dual JAK2/FLT3 Inhibitors for the Treatment of AcuteMyelogenous Leukemia and Myeloproliferative Neoplasms. J Med Chem. 2019 Oct 31.
JAK2/FLT3-IN-1 (TFA) is a potent and orally active dual JAK2/FLT3 inhibitor with IC50 values of 0.7 nM, 4 nM, 26 nM and 39 nM for JAK2, FLT3, JAK1 and JAK3, respectively. JAK2/FLT3-IN-1 (TFA) has anti-cancer activity[1].
IC50 & Target
JAK1
26 nM (IC50)
JAK2
0.7 nM (IC50)
JAK3
39 nM (IC50)
FLT3
4 nM (IC50)
体外研究 (In Vitro)
JAK2/FLT3-IN-1 (0.008-1 μM; for 2 hours) (TFA) down-regulates p-FLT3 in a dose-dependent manner[1]. JAK2/FLT3-IN-1 (5-100 nM; for 2 hours) (TFA) has a dose-dependent effect on the induction of apoptosis in the MV4-11 cells[1]. JAK2/FLT3-IN-1 (5-100 nM; for 2 hours) (TFA) strongly induces cell cycle arrest with a G1/G0 percentage of 85% at 100 nM in the MV4-11 cells[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[1]
Cell Line:
MV4-11 and SET-2 cells
Concentration:
0.008, 0.04, 0.2, 1 μM
Incubation Time:
For 2 hours
Result:
Down-regulated p-FLT3 in a dose-dependent manner from 0.008 to 1 μM.
Apoptosis Analysis[1]
Cell Line:
MV4-11 cells
Concentration:
5, 10, 50, 100 nM
Incubation Time:
For 2 hours
Result:
Had a dose-dependent effect on the induction of apoptosis in the MV4-11 cells.
Cell Cycle Analysis[1]
Cell Line:
MV4-11 cells
Concentration:
5, 10, 50, 100 nM
Incubation Time:
For 2 hours
Result:
Induced cell cycle arrest with a G1/G0 percentage of 85% at 100 nM.
体内研究 (In Vivo)
JAK2/FLT3-IN-1 (30 and 60 mg/kg/day; p.o.; for 14 days) (TFA) exhibits significant antitumor effects[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
NOD/SCID mouse models[1]
Dosage:
30 and 60 mg/kg
Administration:
Oral administration; daily; for 14 days
Result:
Exhibited significant antitumor effects. The tumor growth inhibitory rates (TGI) were respective 58% and 93% in the MV4-11-bearing mice model.
分子量
581.61
Formula
C27H35F4N7O3
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Yang T, et al. Discovery of Potent and Orally Effective Dual JAK2/FLT3 Inhibitors for the Treatment of AcuteMyelogenous Leukemia and Myeloproliferative Neoplasms. J Med Chem. 2019 Oct 31.
CHZ868 is a type II JAK2 inhibitor with an IC50 of 0.17 μM in EPOR JAK2 WT Ba/F3 cell.
IC50 & Target[2]
JAK2
110 nM (IC50)
体外研究 (In Vitro)
CHZ868 potently inhibits constitutive JAK2 and STAT5 phosphorylation in JAK2V617F SET2 cells. CHZ868 potently inhibits the proliferation of SET2 cells (GI50=59nM), and has 6-fold less growth inhibitory activity against CMK cells (GI50=378nM)[1]. At 100 nM CHZ868 has activity against 26 kinases, including JAK2 and TYK2. CHZ868 is thought to engage with the hinge region of JAK2 through two H-bonds, formed between the amino-pyridine of CHZ868 and the backbone-NH/CO of L932, while the pyridine is occupying the adenine pocket of the ATP binding site. CHZ868 potently suppresses the growth of CRLF2-rearranged human B-ALL cells, abrogates JAK2 signaling[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
CHZ868 is characterized by high passive permeability, good metabolic stability, and low water solubility, as well as by moderate blood clearance and good oral bioavailability, making it suitable for in vivo use. CHZ868 improves survival in mice with human or murine B-ALL. CHZ868 and dexamethasone synergistically induces apoptosis in JAK2-dependent B-ALLs and further improves survival compared to CHZ868 alone[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
423.42
Formula
C22H19F2N5O2
CAS 号
1895895-38-1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Meyer SC, et al. CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms. Cancer Cell. 2015 Jul 13;28(1):15-28.
[2]. Wu SC, et al. Activity of the Type II JAK2 Inhibitor CHZ868 in B Cell Acute Lymphoblastic Leukemia. Cancer Cell. 2015 Jul 13;28(1):29-41.
Cell Assay [2]
CHZ868 is dissolved in DMSO to make 10 mM stock solution and diluted in culture media. Cells are treated with CHZ868 (0, 0.05, 0.1, 0.2 μM) or vehicle (DMSO). After 48 hr (Ba/F3 cells) or 72 hr (MHH-CALL4 and PDX cells), CellTiter-Glo Luminescent Cell Viability Assay is added (10 μL undiluted or 25 μL of a 1:2 dilution in each well) and plates are read[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice: CHZ868 is reconstituted in 0.5% methylcellulose / 0.5% Tween-80 and administered at doses of 10 or 30 mg/kg/day by oral gavage. Pharmacokinetic/pharmacodynamic and efficacy studies in the mouse model of rhEpo-induced polycythemia are carried out essentially as reported. Detection of STAT5 phosphorylation in spleen lysates by Meso Scale Discovery is performed[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Meyer SC, et al. CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms. Cancer Cell. 2015 Jul 13;28(1):15-28.
[2]. Wu SC, et al. Activity of the Type II JAK2 Inhibitor CHZ868 in B Cell Acute Lymphoblastic Leukemia. Cancer Cell. 2015 Jul 13;28(1):29-41.
SC99 is an orally active, selective STAT3 inhibitor targeting JAK2-STAT3 pathway. SC99 docks into the ATP-binding pocket of JAK2. SC99 inhibits phosphorylation of JAK2 and STAT3 with no effects on the other kinases associated with STAT3 signaling. SC99 inhibits platelet activation, aggregation and displays potent anti-myeloma, anti-thrombotic activities[1][2][3].
IC50 & Target
STAT3
JAK2
体外研究 (In Vitro)
SC99 (10 or 30 μM; for 72 hours) induces MM cell death[1]. SC99 (10 μM; 24 hours) decreases the p-STAT3 level but has no effects on total STAT3 expression. SC99 (2.5, 5, 10, 20 μM; for 60 mins) inhibits JAK2 phosphorylation in a concentration-dependent manner but does not inhibit the phosphorylation levels of AKT, ERK, mTOR or c-Src at a concentration up to 20 μM[1]. SC99 (1.25, 2.5, 5 μM; pre-treated for 10 min) inhibits collagen (2 μg/mL) and thrombin (0.02 U/mL) induced phosphorylation of STAT3 in a concentration-dependent manner[2]. SC99 (pre-treated for 2 hours) inhibits IL-6 (50 ng/ml; for 20 min) induced STAT3 nuclear translocation in OPM2 cells[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Apoptosis Analysis[1]
Cell Line:
Six multiple myeloma (MM) cell lines (LP1, JJN3, RPMI-8226, U266, OPM2 and OCI-MY5)
Concentration:
10 or 30 μM
Incubation Time:
For 72 hours
Result:
Induced MM cell death.
Apoptosis Analysis[1]
Cell Line:
MM cell lines[1]
Concentration:
10 μM
Incubation Time:
24 hours
Result:
Decreased the p-STAT3 level but had no effects on total STAT3 expression in all cell lines examined.
体内研究 (In Vivo)
SC99 (30 mg/kg; orally; daily; for continuous 14 or 28 days) delays myeloma tumor growth in xenograft mice models[1]. SC99 (5, 10, 15 mM, 15 μL; ICV) produces an effective inhibitory effect on the phosphorylation of JAK2 and STAT3 in middle cerebral artery occlusion and reperfusion (MCAO/R) model (adult male SD rats; 250-300 g). SC99 ameliorates neuronal apoptosis and degeneration, neurobehavioral deficits, inflammatory response and brain edema[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Nude mice with Human MM cells OPM2 or JJN3[1]
Dosage:
30 mg/kg
Administration:
Orally; daily; for continuous 14 or 28 days
Result:
Delayed myeloma tumor growth in xenograft mice models and suppressed tumor growth more than 40% in 14 days in the OPM2 model.
分子量
336.15
Formula
C15H8Cl2FN3O
CAS 号
882290-02-0
运输条件
Room temperature in continental US; may vary elsewhere.
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Zubin Zhang, et al. A novel small molecule agent displays potent anti-myeloma activity by inhibiting the JAK2-STAT3 signaling pathway. Oncotarget. 2016 Feb 23;7(8):9296-308.
[2]. Zhuan Xu, et at. A novel STAT3 inhibitor negatively modulates platelet activation and aggregation. Acta Pharmacol Sin. 2017 May;38(5):651-659.
[3]. Yiping Ding, et al. Effects of SC99 on cerebral ischemia-perfusion injury in rats: Selective modulation of microglia polarization to M2 phenotype via inhibiting JAK2-STAT3 pathway. Neurosci Res. 2019 May;142:58-68.
NSC 42834 (JAK2 Inhibitor V), a novel specific inhibitor of Jak2, inhibits Jak2-V617F and Jak2-WT autophosphorylation in a dose-dependent manner but was not cytotoxic to cells at concentrations that inhibited kinase activity.
IC50 & Target
JAK2-WT
15 μM (IC50)
JAK2-V617F
28 μM (IC50)
体外研究 (In Vitro)
NSC 42834 (JAK2 Inhibitor V) selectively inhibited Jak2 kinase function with no effect on Tyk2 or c-Src kinase function. NSC 42834 significantly inhibited proliferation of the Jak2-V617F-expressing, human erythroleukemia cell line, HEL 92.1.7. The NSC 42834-mediated reduction in cell proliferation correlated with reduced Jak2 and STAT3 tyrosine phosphorylation levels as well as marked cell cycle arrest. Finally, NSC 42834 inhibited the growth of hematopoietic progenitor cells isolated from the bone marrow of an essential thrombocythemia patient harboring the Jak2-V617F mutation and a polycythemia vera patient carrying a Jak2-F537I mutation.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
344.45
Formula
C23H24N2O
CAS 号
195371-52-9
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Jacqueline Sayyah, Andrew Magis, David A. Ostrov, et al. Z3, a novel Jak2 tyrosine kinase small-molecule inhibitor that suppresses Jak2-mediated pathologic cell growth . Mol Cancer Ther 2008;7(8):2308-18.
[2]. Jacqueline Sayyah, Peter P. Sayeski. Jak2 inhibitors: Rationale and role as therapeutic agents in hematologic malignancies. Current Oncology Reports. 2009, 11(2): 117-124.
[3]. Ehab Atallah , Srdan Verstovsek . Prospect of JAK2 inhibitor therapy in myeloproliferative neoplasms. Expert Review of Anticancer Therapy. 2009,9 (5):663-670.
