| Identification | Back Directory | [Name]
3,9-bis((ethylthio)methyl)-K-252a | [CAS]
156177-65-0 | [Synonyms]
Kt7515
Kt-7515
C106592
Cep1347
Kt 7515
Cep-1347
Cep 1347
9-Bis(etsm)-K-252a
CEP-1347
(KT-7515
3,9-Bis(etsm)-K-252a
SCMLRESZJCKCTC-KMYQRJGFSA-N
3,9-bis((ethylthio)methyl)-K-252a
3;9-BIS(ETSM)-K-252A; CEP 1347; CEP-1347; CEP1347; KT 7515
9,12-Epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylicacid,5,16-bis[(ethylthio)methyl]-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-,methyl ester, (9S,10R,12
(9S,10R,12R)-5-16-Bis[(ethylthio)methyl]-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester
9,12-Epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid, 5,16-bis[(ethylthio)methyl]-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-, methyl ester, (9S,10R,12R)- | [Molecular Formula]
C33H33N3O5S2 | [MDL Number]
MFCD27991285 | [MOL File]
156177-65-0.mol | [Molecular Weight]
615.76 |
| Chemical Properties | Back Directory | [Boiling point ]
786.8±60.0 °C(Predicted) | [density ]
1.53±0.1 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
<6.16mg/ml in DMSO | [form ]
solid | [pka]
11.94±0.40(Predicted) | [color ]
Pale yellow |
| Hazard Information | Back Directory | [Uses]
CEP 1347 (cas# 156177-65-0) is a useful research chemical.CEP 1347 promotes neuronal survival in culture and in vivo. | [Biological Activity]
cep-1347, also called kt 7515, is an inhibitor of the c-jun n-terminal kinase (jnk) signaling pathway, with an ic50 value for jnk1 activation of 20 ± 2 nm in rat embryonic motoneurons [1].the jnk pathway, also known as the stress-activated protein kinase (sapk) pathway, is one of the signaling cascades that mediate the apoptotic death in response to a variety of stressful stimuli. jnk activation by phosphorylation is important for neuronal cell death after injury in vivo and after trophic factor withdrawal in vitro [2].cep-1347 induced neuronal survival. jnk1 activity in untreated cell cultures increased approximately fourfold within 24 hr after plating. as early as 15 min after the application of cep-1347 at 500 nm, the activity of jnk1 sharply decreased to ~50% of control levels. for the next 24 hr, the activity of jnk1 continued to decrease. cultures rich in motoneurons were grown in the presence of cep-1347 at increasing concentrations, and the ic50 for jnk1 activity at 22 hr was 21 ± 2 nm, whereas the ec50 for cell survival at 5 d was 20 ± 2 nm [1].cep-1347 can affect noise-induced hearing loss. data showed that hearing thresholds 2 d before noise exposure showed no significant difference between the noise-exposed control and treated group. hearing threshold shifts in all guinea pigs 2 d after the noise exposure. by day 6 after exposure, threshold shifts were significantly less in the cep-1347 group than in the noise-exposed control group. by 2 weeks after exposure, the difference between the two groups became more pronounced [2]. | [in vivo]
CEP-1347 (0-60 mg/kg; Subcutaneous injection (s.c.)) in rats treated with Caerulein (HY-A0190) (10 μg/kg; Intravenous injection (i.v.)) can dose-dependent inhibit Caerulein Induced JNK activation and improve pancreatitis induced by pancreatin[6].
| Animal Model: | male white Sprague-Dawley rats[6] | | Dosage: | Caerulein (HY-A0190): 10 μg/kg; CEP-1347: 0-60 mg/kg | | Administration: | Caerulein: Intravenous injection (i.v.); CEP-1347: Subcutaneous injection (s.c.) | | Result: | Caerulein-induced JNK activation was dose-dependent inhibited. |
| [IC 50]
JNK1 | [storage]
Store at -20°C | [References]
[1]. maroney ac, glicksman ma, basma an, et al. motoneuron apoptosis is blocked by cep-1347 (kt 7515), a novel inhibitor of the jnk signaling pathway[j]. the journal of neuroscience, 1998, 18(1): 104-111.
[2]. pirvola u, liang xq, virkkala j, et al. rescue of hearing, auditory hair cells, and neurons by cep-1347/kt7515, an inhibitor of c-jun n-terminal kinase activation[j]. the journal of neuroscience, 2000, 20(1): 43-50. |
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