Scriptaid 287383-59-9

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Molecular Weight:

326.35 Scriptaid is an inhibitor of HDAC. It shows a greater effect on acetylated H4 than H3.


Biological Activity


Scriptaid (6 μM) results in a >100-fold increase in histone
acetylation in PANC-1 cell. Scriptaid (8 μM) is not lethal to PANC-1
cell and has limited effects (80% survival) on MDAMB-468. Scriptaid
increases the transcription of pCMVb, p6SBE-luc and p6MBE-luc
independent of a positive inducer of transcription.


Scriptaid is capable
of inducing high expression of p6MBE-luc, pCMVb, and pUB6/V5-LacZ,
driven by viral (SV40 and CMV) or human (Ubiquitin c, UB6) promoters,
which do not depend on the specificity of the enhancer (SBE versus MBE),
the type of promoter (viral versus cellular), the product of the
reporter gene (luciferase versus b-gal), nor on the integration status
of the reporter construct.


Scriptaid induces high rates
of somatic cell nuclear transfer (SCNT) oocytes development to the
blastocyst stage and allowed full-term development (3.4, 4.2, 7.6, 6.8,
and 4.1%) with all concentrations (50, 100, 250, 500, and 2000 nM
respectively). Scriptaid improves the full-term development of cloned
B6D2F1embryos in a dose-dependent manner with the maximum effect at 250
nM.


Scriptaid enables the clone of all the important inbred mouse
strains, such as C57BL/6, C3H/He, DBA/2, and 129/Sv. Scriptaid treatment
enhances newly synthesized mRNA levels in cloned embryos. 250 nM
Scriptaid treated for up to 48 h, does not inhibit the development of
ICSI-fertilized embryos.


Scriptaid inhibits T. gondii tachyzoite proliferation with IC50 of 39 nM. Scriptaid (0.225 μM) completely protects the HS68 monolayers from T. gondii tachyzoite. Scriptaid inhibits growth of ER negative cell lines, MDA-MB-231,
MDA-MB-435 and Hs578t with IC50 of 0.5-1.0 μg/mL after 48 h treatment. 1
μg/ml Scriptaid treated for 48 h induces an accumulation of both
acetylated H3 and acetylated H4 histone tail Proteins, and a maximal of
20,000-fold increase of ER mRNA transcript.


Scriptaid
inhibits the proliferation and viability of the Ishikawa endometrial
cancer cell line, and the SK-OV-3 ovarian cancer cell line with IC50 of 9
μM and 55 μM, respectively, while the normal human endometrial
epithelial cells shows little sensitivity. Endometrial cancer cells and
ovarian cancer cells cultured for 2 days in the presence of Scriptaid
shows an accumulation in the G0/G1 phase (5 μM of Scriptaid) and G2/M
phase (10 μM of Scriptaid) of the Cell Cycle, with a concomitant
decrease in the proportion of those in the S phase. 10 μM of Scriptaid
induces a 56.1% of apoptotic Ishikawa cells with loss of mitochondrial
membrane potential, and decreased levels of cyclin A and bcl-2 levels by
50% and 20%, respectively.






Scriptaid elicits a dose-dependent decrease in lesion size (a maximal
decrease of 45%) at 1.5 to 5.5 mg/kg and a concomitant attenuation in
motor and cognitive deficits when delivered 30 minutes postinjury in a
model of mode rate TBI. Comparable protection is achieved even when
treatment is delayed to 12 h postinjury.


The protection of motor and
cognitive functions is long lasting, as similar improvements are
detected 35 days postinjury. Scriptaid induces an increase in surviving
neurons (42%), as well as the number/length of their processes within
the CA3 region of the hippocampus and the pericontusional cortex.


Scriptaid treatment prevents the decrease in phospho-AKT (p-AKT) and
phosphorylated phosphatase and tensin homolog deleted on chromosome 10 (
p-PTEN) induced by TBI in cortical and CA3 hippocampal neurons. Scriptaid treatment (3.5 mg/kg) clearly inhibits tumor growth in a
human breast cancer xenograft MDA-MB-231 model, reducing tumor volume by
75%.

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Product Categories : Epigenetics > HDAC Inhibitor