156177-65-0 Usage
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].
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.
Check Digit Verification of cas no
The CAS Registry Mumber 156177-65-0 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 1,5,6,1,7 and 7 respectively; the second part has 2 digits, 6 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 156177-65:
(8*1)+(7*5)+(6*6)+(5*1)+(4*7)+(3*7)+(2*6)+(1*5)=150
150 % 10 = 0
So 156177-65-0 is a valid CAS Registry Number.
InChI:InChI=1/C33H33N3O5S2/c1-5-42-15-17-7-9-23-19(11-17)27-28-21(14-34-31(28)37)26-20-12-18(16-43-6-2)8-10-24(20)36-30(26)29(27)35(23)25-13-22(32(38)41-39-4)33(36,3)40-25/h7-12,22,25H,5-6,13-16H2,1-4H3,(H,34,37)/t22-,25+,33+/m1/s1
156177-65-0Relevant articles and documents
Neurotrophic 3,9-bis[(alkylthio)methyl]-and-bis(alkoxymethyl)-K-252a derivatives
Kaneko, Masami,Saito, Yutaka,Saito, Hiromitsu,Matsumoto, Tadashi,Matsuda, Yuzuru,Vaught, Jeffry L.,Dionne, Craig A.,Angeles, Thelma S.,Glicksman, Marcie A.,Neff, Nicola T.,Rotella, David P.,Kauer, James C.,Mallamo, John P.,Hudkins, Robert L.,Murakata, Chikara
, p. 1863 - 1869 (1997)
A series of 3,9-disubstituted [(alkylthio)methyl]- and (alkoxymethyl)- K-252a derivatives was synthesized with the aim of enhancing and separating the neurotrophic properties from the undesirable NGF (trk A kinase) and PKC inhibitory activities of K-252a. Data from this series reveal that substitution in the 3- and 9-positions of K-252a with these groups reduces trk A kinase inhibitory properties approximately 100- to >500-fold while maintaining or in certain cases enhancing the neurotrophic activity. From this research, 3,9-bis[(ethylthio)methyl]-K-252a (8) was identified as a potent and selective neurotrophic agent in vitro as measured by enhancement of choline acetyltransferase activity in embryonic rat spinal cord and basal forebrain cultures. Compound 8 was found to have weak kinase inhibitory activity for trk A, protein kinase C, protein kinase A, and myosin light chain kinase. On the basis of the in vitro profile, 8 was evaluated in in vivo models suggestive of neurological diseases. Compound 8 was active in preventing degeneration of cholinergic neurons of the nucleus basalis magnocellularis (NBM) and reduced developmentally programmed cell death (PCD) of female rat spinal nucleus of the bulbocavernosus motoneurons and embryonic chick lumbar motoneurons.
