3,9-bis((ethylthio)methyl)-K-252a

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3,9-bis((ethylthio)methyl)-K-252a Basic information
Product Name:3,9-bis((ethylthio)methyl)-K-252a
Synonyms:3,9-bis((ethylthio)methyl)-K-252a;3,9-Bis(etsm)-K-252a;C106592;Cep 1347;Cep1347;Cep-1347;Kt 7515;Kt7515
CAS:156177-65-0
MF:C33H33N3O5S2
MW:615.77
EINECS:
Product Categories:
Mol File:156177-65-0.mol
3,9-bis((ethylthio)methyl)-K-252a Structure
3,9-bis((ethylthio)methyl)-K-252a Chemical Properties
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
pka11.94±0.40(Predicted)
color Pale yellow
Safety Information
HS Code 2922500090
MSDS Information
3,9-bis((ethylthio)methyl)-K-252a Usage And Synthesis
UsesCEP 1347 (cas# 156177-65-0) is a useful research chemical.CEP 1347 promotes neuronal survival in culture and in vivo.
Biological Activitycep-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 50JNK1
storageStore 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.
3,9-bis((ethylthio)methyl)-K-252a Preparation Products And Raw materials
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