Details
| Stereochemistry | ACHIRAL |
| Molecular Formula | C18H18F3N3O |
| Molecular Weight | 349.3502 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
FC(F)(F)C1=CC(NC(=O)C2=CC=NC=C2)=C(C=C1)N3CCCCC3
InChI
InChIKey=DWFGGOFPIISJIT-UHFFFAOYSA-N
InChI=1S/C18H18F3N3O/c19-18(20,21)14-4-5-16(24-10-2-1-3-11-24)15(12-14)23-17(25)13-6-8-22-9-7-13/h4-9,12H,1-3,10-11H2,(H,23,25)
| Molecular Formula | C18H18F3N3O |
| Molecular Weight | 349.3502 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
SRPIN340 was investigated as selective serine arginine protein kinase (SRPK) 1 inhibitor, it also could inhibit SRPK2 at higher concentrations, but did not significantly inhibit other SRPKs such as CLK1 and CLK4, or other classes of SR kinases. It was shown, that SRPIN340 targeted host proteins, and might be effective against multiple hepatitis C virus (HCV) genotypes. Furthermore, the toxicity data available for SRPIN340 were promising and no adverse effects were observed when SRPIN340 was administered orally to rats. On the other hand, the fact that this inhibitor acted through cellular components still raises concerns regarding its safety in the case of human use. Future studies with SRPIN340, its derivatives, and other chemicals that target SRPKs could be directed toward developing a new class of antiviral treatment regimens and drugs.
Originator
Approval Year
PubMed
| Title | Date | PubMed |
|---|---|---|
| SRPK1 inhibition modulates VEGF splicing to reduce pathological neovascularization in a rat model of retinopathy of prematurity. | 2013-08-27 |
|
| SRPK1 inhibition in vivo: modulation of VEGF splicing and potential treatment for multiple diseases. | 2012-08 |
|
| Utilization of host SR protein kinases and RNA-splicing machinery during viral replication. | 2006-07-25 |
Sample Use Guides
in rats (toxicity effect): No adverse effects were observed when SRPIN340 was orally administrated to rats, even at the highest SRPIN340 dose (2,000 mg/kg). 10 rats were observed for 2 weeks after SRPIN340 administration. All of the rats survived,
Route of Administration:
Oral
SRPIN340 (40 μM) rescues Vero cells from the cytopathic effect of Sindbis virus. In a plaque assay with Vero cells, the SRPIN340 IC50 for Sindbis virus propagation was 60 μM. Preliminary studies indicate that SRPIN340 also suppresses propagation of severe acute respiratory syndrome virus. Thus, the kinase activities of SR protein kinase (SRPKs) appear to be required for propagation of a variety of RNA viruses. SRPIN340 in a dose-dependent manner (0, 10, 20 and 50 uM) inhibits SR phosphorylation by SRPK in Flp-In293 cells and promotes degradation of SRp75. Thus, because retention of SRp75 is necessary for HIV expression, SRPIN340 emerges as a potential inhibitor of HIV production
| Substance Class |
Chemical
Created
by
admin
on
Edited
Wed Apr 02 05:49:27 GMT 2025
by
admin
on
Wed Apr 02 05:49:27 GMT 2025
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| Record UNII |
9QS4MR9N9D
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| Record Status |
Validated (UNII)
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| Record Version |
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