SRSF1-IN-1
SRSF1-IN-1 is a SRSF1 inhibitor. SRSF1-IN-1 inhibits SRSF1 expression, thereby modulating the splicing of Bcl-x pre-mRNA. SRSF1-IN-1 inhibits the proliferation of various cancer cells. SRSF1-IN-1 induces apoptosis in gastric cancer cells, reduces Bcl-xl expression, and upregulates cleaved PARP and caspase 3. SRSF1-IN-1 induces autophagy and promotes cell death. SRSF1-IN-1 exhibits anti-tumor activity in a mouse gastric cancer xenograft model. SRSF1-IN-1 can be used for the research of various cancers including liver cancer, gastric cancer, breast cancer, colon cancer, glioma, and melanoma.
For research use only. We do not sell to patients.
- Formula: C20H24O5S
- Molecular Weight:376.47
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Biological Activity
SRSF1-IN-1 (STP2) (72 h) potently inhibits the proliferation of HepG2, MCF7, HCT116, U251, HGC27, AGS, BGC823, SGC7901, A549 and B16F10 cell lines, with IC50 values of 0.63, 1.79, 0.52, 2.43, 0.62, 1.03, 1.3, 1.88, >10 and 1.03 μM, respectively. It also exhibits selective toxicity toward tumor cells compared with normal human LO2 hepatocytes[1].
SRSF1-IN-1 (0.5-2 μM; 48 h) induces dose-dependent apoptosis in HGC27 and AGS gastric cancer cells, increases the proportion of apoptotic cells, downregulates the anti-apoptotic protein Bcl-xl, and upregulates cleaved PARP and cleaved caspase 3[1].
SRSF1-IN-1 (0.5-2 μM; 24 h) arrests HGC27 and AGS gastric cancer cells at the S phase, accompanied by upregulated expression of the P21 protein and downregulated expression of the CyclinE2 protein[1].
SRSF1-IN-1 (0.5-2 μM; 24 h) downregulates SRSF1 mRNA and protein expression in a dose-dependent manner in HGC27 and AGS gastric cancer cells; at the concentration of 2 μM, it inhibits the RNA splicing pathway in HGC27 cells and upregulates autophagy-related genes[1].
SRSF1-IN-1 (0.5-2 μM; 48 h) induces autophagy in HGC27 and AGS gastric cancer cells; when combined with 2 μM Chloroquine (CQ) (HY-17589A) for 24 h, it also enhances the formation of LC3B puncta[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HGC27, AGS
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Induced apoptosis in a dose-dependent manner: in HGC27 cells, apoptosis proportion increased from 8.15% to 47.8%; in AGS cells, apoptosis proportion increased from 7.59% to 63.3%.
Reduced anti-apoptotic Bcl-xl protein expression and increased cleaved-PARP and cleaved-caspase 3 expression in both cell lines.
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Cell Line:HGC27, AGS
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:24 h
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Result:Increased the proportion of S-phase cells: in HGC27 cells, S-phase proportion rose from 50.19% to 75.34%; in AGS cells, S-phase proportion rose from 32.86% to 52.16%.
Increased P21 protein expression and reduced CyclinE2 protein expression in both cell lines, with no obvious dose dependence.
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Cell Line:HGC27, AGS
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:24 h
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Result:Showed significant downregulation of the RNA splicing pathway, reduced mRNA expression of SRSF1, and increased expression of autophagy-related genes (BECN1, MAP1LC3B, MAP1LC3B2) in HGC27 cells treated with 2 μM.
Confirmed dose-dependent reduction of SRSF1 mRNA levels in both HGC27 and AGS cells.
Showed corresponding dose-dependent reduction of SRSF1 protein levels in both cell lines.
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Cell Line:HGC27, AGS
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h (Western blot); 24 h (immunofluorescence)
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Result:Increased ATG5, Beclin1, and LC3 II/LC3 I ratio, and decreased P62 protein levels in both HGC27 and AGS cells at 0.5, 1, and 2 μM for 48 h.
Resulted in a significant increase in LC3B puncta in HGC27 cells when combined with CQ (20 μM) for 24 h at 2 μM.
STP2 (1 g/kg; i.p.; single dose) is well-tolerated in male ICR mice, with 100% survival, gradual weight gain, and no apparent liver histopathological abnormalities over 7 days[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (male, 6 weeks old, gastric cancer xenograft model with HGC27 cells)[1]
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Dosage:25 mg/kg; 100 mg/kg
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Administration:i.p.; daily; 15 days
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Result:Suppressed tumor growth in a dose-dependent manner, with tumor growth inhibition (TGI) values of 63.68% at 25 mg/kg and 82.66% at 100 mg/kg.
Caused no apparent body weight loss during the 15-day treatment period.
Reduced P62 protein levels and increased LC3B protein levels (a marker of autophagy) in HGC27 tumor tissues from treated mice.
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Animal Model:ICR (male)[1]
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Dosage:1 g/kg
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Administration:i.p.; single dose
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Result:Resulted in 100% survival of mice over the 7-day observation period.
Led to gradual weight gain in mice over the 7-day duration.
Caused no obvious abnormal changes in hepatocyte morphology in liver tissues, with no enlarged volume, empty/bright cytoplasm, or unclear cell boundaries observed.
Chemical Information
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Molecular Weight 376.47
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Formula C20H24O5S
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SMILES
S=C1OCC2=C1CC[C@@]3(C)[C@@]2([H])C[C@H](O4)[C@]54[C@@]3(O6)[C@@H]6[C@H]7[C@@](O7)(C(C)C)[C@H]5O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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