1128096-91-2
Chemical Structure
SR-3306
- CAS No.: 1128096-91-2
- Formula:C28H26N8O
- Molecular Weight:490.56
IUPAC Name: N-(4-(3-(6-methylpyridin-3-yl)-1H-1,2,4-triazol-1-yl)phenyl)-4-(3-morpholinophenyl)pyrimidin-2-amine
InChIKey: QDMXVKKPYBGIAS-UHFFFAOYSA-N
SMILES: CC(C=C1)=NC=C1C2=NN(C=N2)C3=CC=C(NC4=NC=CC(C5=CC=CC(N6CCOCC6)=C5)=N4)C=C3
Biological Activity: SR-3306 is a brain-penetrant and selective pan-JNK (JNK1/2/3) inhibitor. SR-3306 is a neuroprotective agent that can be used for the study of Parkinson's disease, ischemia/reperfusion (I/R) injury and obesity[1][2][3].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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SR-3306 | 98.01% | SR-3306 is a brain-penetrant and selective pan-JNK (JNK1/2/3) inhibitor. SR-3306 is a neuroprotective agent that can be used for the study of Parkinson's disease, ischemia/reperfusion (I/R) injury and obesity. | ||||||||||||||||||||
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JNK-9L | 98.06% | JNK-9L (Compound 9l) is a BBB-penetrable and ATP-competitive JNK inhibitor with IC50s of 0.099 and 0.148 μM for JNK1 and JNK3, respectively. JNK-9L significantly inhibits c-jun phosphorylation and Streptozotocin (HY-13753)-induced ROS generation with an IC50 of 0.8 nM. JNK-9L can be used for neurodegenerative disorders like Parkinson’s disease research. | ||||||||||||||||||||
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Momelotinib (Standard) | ≥98% | Momelotinib (Standard) is the analytical standard of Momelotinib. This product is intended for research and analytical applications. Momelotinib (CYT387) is an ATP-competitive inhibitor of JAK1/JAK2 with IC50a of 11 nM and 18 nM,respectively. CYT387 shows much less activity against JAK3. | ||||||||||||||||||||
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Momelotinib mesylate | Momelotinib mesylate (CYT387 mesylate) is an ATP-competitive inhibitor of JAK1/JAK2 with IC50 of 11 nM/18 nM, appr 10-fold selectivity versus JAK3. | |||||||||||||||||||||
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TBK1/IKKε-IN-2 | 98.62% | TBK1/IKKε-IN-2 is a dual TBK1 and IKKε inhibitor. | ||||||||||||||||||||
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XL019 | 99.65% | 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. | ||||||||||||||||||||
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JAK3-IN-11 | JAK3-IN-11 (Compound 12), a potent, noncytotoxic, irreversible, orally active JAK3 inhibitor with IC50 value of 1.7 nM, has excellent selectivity (>588-fold compared to other JAK isoforms), covalently bind to the ATP-binding pocket in JAK3. JAK3-IN-11 strongly inhibits JAK3-dependent signaling and T cell proliferation, is a promising tool for study autoimmune diseases. | |||||||||||||||||||||
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ALK5-IN-33 | ALK5-IN-33 (Compound EX-10) is a selective, orally active ALK-5 inhibitor with an IC50 ≤10 nM. | |||||||||||||||||||||
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JNK-IN-17 | JNK-IN-17 (Compound 9J) is a selective and potent JNK inhibitor with IC50 values of 0.039, 0.079 μM for JNK1 and JNK3. JNK-IN-17 can inhibit c-Jun phosphorylation with an IC50 of 0.082 μM in Streptozotocin (HY-13753)-infuced INS-1 pancreatic islet β cells. JNK-IN-17 shows inhibition rate ≤ 33% on the four main P450 subtypes (2C9, 2D6, 3A4, 1A2) in human liver microsomes, indicating a relatively low risk of drug interactions. JNK-IN-17 can be used for researches of neurological and metabolic disease, such as Parkinson's disease. | |||||||||||||||||||||
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4-(2-(4-Morpholinophenylamino)pyrimidin-4-yl)benzoic acid | 98.91% | 4-(2-(4-Morpholinophenylamino)pyrimidin-4-yl)benzoic acid is a drug intermediate for synthesis of various active compounds. | ||||||||||||||||||||
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Momelotinib dihydrochloride | 99.56% | Momelotinib (dihydrochloride) is a JAK1/JAK2 inhibitor that also antagonizes ACVR1, leading to downregulation of Hepcidin expression and increased availability of iron for erythropoiesis. Momelotinib (dihydrochloride) can reduce transfusion burden and spleen enlargement caused by myelofibrosis, showing potential value in research and application within the field of myelofibrosis. | ||||||||||||||||||||
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References
- [1]. Crocker CE, et al. JNK Inhibition Protects Dopamine Neurons and Provides Behavioral Improvement in a Rat 6-hydroxydopamine Model of Parkinson's Disease. ACS Chem Neurosci. 2011 Apr 20;2(4):207-212. [Content Brief]
- [2]. Gao S, et al. Pharmacological Inhibition of c-Jun N-terminal Kinase Reduces Food Intake and Sensitizes Leptin's Anorectic Signaling Actions. Sci Rep. 2017 Feb 6;7:41795. [Content Brief]
- [3]. Chambers JW, et al. Inhibition of JNK mitochondrial localization and signaling is protective against ischemia/reperfusion injury in rats. J Biol Chem. 2013 Feb 8;288(6):4000-11. [Content Brief]