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SRPIN340 (CAS 218156-96-8) LS-H125

SRPK1 inhibitor
LS-H125-1 / 1 mg / $175
LS-H125-5 / 5 mg / $205
LS-H125-10 / 10 mg / $245
LS-H125-25 / 25 mg / $355
USA Shipment Only
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Description: Serine/arginine-rich protein kinase 1 (SRPK1) targets proteins that contain multiple serine/arginine (SR) dipeptides, including SR-rich splicing factor 1, SRSF1. SRPIN340 is an isonicotinamide compound that inhibits SRPK1 (Ki = 0.89 µM). It is about 10-fold less effective against SRPK2 and does not inhibit the related SRPKs, Clk1 and Clk4. SRPIN340 suppresses the propagation of Sindbis virus in Vero cells and the replication of hepatitis C virus in Huh7/Rep-Feo-2a cells. By blocking SRPK1-mediated phosphorylation of SRSF1, SRPIN340 modulates alternative splicing of VEGF, reducing neovascularization both in cells and in animals. H125_ChemicalStructureImage.png
SRPK Inhibitor
biochemical, chemical, inhibitor
A crystalline solid
Shipped Ambient, store at -20°C, ≥ 2 years shelf life.
This product is for research use only. Not for administration to humans, or for human or veterinary diagnostic or therapeutic use.
Data Sheet DataSheet    SDS SDS
Related Products: SRPK1 related products

Usage Information

SRPIN340 is supplied as a crystalline solid. A stock solution may be made by dissolving the SRPIN340 in the solvent of choice. SRPIN340 is soluble in organic solvents such as ethanol, DMSO, and dimethyl formamide (DMF), which should be purged with an inert gas. The solubility of SRPIN340 in ethanol and DMF is approximately 25 mg/ml and approximately 15 mg/ml in DMSO. SRPIN340 is sparingly soluble in aqueous buffers. For maximum solubility in aqueous buffers, SRPIN340 should first be dissolved in ethanol and then diluted with the aqueous buffer of choice. SRPIN340 has a solubility of approximately 0.2 mg/ml in a 1:4 solution of ethanol:PBS (pH 7.2) using this method. We do not recommend storing the aqueous solution for more than one day.

  1. Ghosh, G. and Adams, J.A. Phosphorylation mechanism and structure of serine-arginine protein kinases. FEBS J. 278(4), 587-597 (2011).
  2. Fukuhara, T., Hosoya, T., Shimizu, S., et al. Utilization of host SR protein kinases and RNA-splicing machinery during viral replication. Proc. Natl. Acad. Sci. USA 103(30), 11329-11333 (2006).
  3. Karakama, Y., Sakamoto, N., Itsui, Y., et al. Inhibition of hepatitis C virus replication by a specific inhibitor of serinearginine-rich protein kinase. Antimicrob. Agents Chemother. 54(8), 3179-3186 (2010).
  4. Ghadimi, M.P., Lopez, G., Torres, K.E., et al. Targeting the PI3K/mTOR axis, alone and in combination with autophagy blockade, for the treatment of malignant peripheral nerve sheath tumors. Mol. Cancer Ther. 11(8), 1758-1769 (2012).
  5. Gammons, M.V.R., Dick, A.D., Harper, S.J., et al. SRPK1 inhibition modulates VEGF splicing to reduce pathological neovascularization in a rat model of retinopathy of prematurity. Invest. Ophthalmol. Vis. Sci. 54(8), 5797-5806 (2013).


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