| Company Name: |
NCE Biomedical Co.,Ltd. |
| Tel: |
4000-027-021 |24 +86-13986109188 | +86-15623472865 | +81-08033611988 |
| Email: |
|
- CC-401
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- $1680.00
-
2026-07-15
- CAS:395104-30-0
- Purity:
- Supply Ability: 10g
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| | 3-[3-[2-(1-Piperidinyl)ethoxy]phenyl]-5-(1H-1,2,4-triazol-5-yl)-1H-indazole Basic information |
| | 3-[3-[2-(1-Piperidinyl)ethoxy]phenyl]-5-(1H-1,2,4-triazol-5-yl)-1H-indazole Chemical Properties |
| Boiling point | 681.5±65.0 °C(Predicted) | | density | 1.275 | | storage temp. | Store at -20°C | | solubility | ≥19.4 mg/mL in DMSO; ≥2.32 mg/mL in EtOH with ultrasonic; ≥8.7 mg/mL in H2O | | form | solid | | pka | 9.44±0.20(Predicted) |
| | 3-[3-[2-(1-Piperidinyl)ethoxy]phenyl]-5-(1H-1,2,4-triazol-5-yl)-1H-indazole Usage And Synthesis |
| Description | c-Jun N-terminal kinases (JNKs) are MAP kinase family members that become highly activated after cells are exposed to stress conditions and are poorly activated by exposure to growth factors or mitogens. CC-401 is a potent inhibitor of all three JNK isoforms (Ki values range from 25 to 50 nM). It has at least 40-fold selectivity for JNK compared with other related kinases. CC-401 is bioavailable when delivered by gavage, blocking JNK signaling and renal fibrosis in a rat obstructed kidney model. It also has been shown to decrease hepatic necrosis and apoptosis after orthotopic liver transplantation and prevent acute renal failure following ischemia/reperfusion associated with renal transplantation in rats. | | Uses | CC-401 inhibits c-JUN N-terminal kinases (JNKs) by binding to its ATP-binding site. JNKs belong to the MAP kinase family and respond to stress signals such as heat, cytokines, and osmotic shock. | | Definition | ChEBI: 3-[3-[2-(1-piperidinyl)ethoxy]phenyl]-5-(1H-1,2,4-triazol-5-yl)-1H-indazole is a member of pyrazoles and a ring assembly. | | in vivo | The staining of p-JNK is moderately induced in bevazicumab and Oxaliplatin treatments as compared to control, and in the CC-401-treated samples p-cJun content is significantly lower, consistent with effective JNK inhibition. DNA damage is modestly elevated in combined treatments with CC-401[2]. CC-401 treatment from days 7 to 24 slows the progression of proteinuria, which is significantly reduced compared to the no-treatment and vehicle groups at days 14 and 21. However, there is still an increase in the degree of proteinuria at day 21 in CC-401-treated rats compared to proteinuria at day 5. The vehicle and no-treatment groups developed renal impairment at day 24 as shown by an increase in serum creatinine. This is prevented by CC-401 treatment[3]. | | IC 50 | JNK: 25-50 nM (Ki) | | references | [1] ma f y, flanc r s, tesch g h, et al. a pathogenic role for c-jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. journal of the american society of nephrology, 2007, 18(2): 472-484.
[2] flanc r s, ma f y, tesch g h, et al. a pathogenic role for jnk signaling in experimental anti-gbm glomerulonephritis. kidney international, 2007, 72(6): 698-708.
[3] bogoyevitch m a, arthur p g. inhibitors of c-jun n-terminal kinases—junk no more biochimica et biophysica acta (bba)-proteins and proteomics, 2008, 1784(1): 76-93. |
| | 3-[3-[2-(1-Piperidinyl)ethoxy]phenyl]-5-(1H-1,2,4-triazol-5-yl)-1H-indazole Preparation Products And Raw materials |
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