SR-1815

SR-1815 (5 nM-10 µM; 3-5 days) exhibits antiproliferative activity in multiple cancer cell lines, with the strongest potency in MV-4-11 cells (EC₅₀ = 0.008 µM)^[2].
SR-1815 is a relatively selective multi-kinase inhibitor, and its KinomeSCAN profile is similar to that of the reference drug^[3].
SR-1815 shows approximately 1000-fold antiproliferative selectivity for cancer cell lines relative to standard cell lines^[3].
SR-1815 shows antiproliferative EC₅₀ values: 0.4 µM in GIST-T1, 0.008 µM in MV-4-11, 9.5 µM in A549, 7.1 µM in MCF7, and 5.4 µM in MDA-MB-468^[4].

SR-1815 increases SynGAP, PSD-95, GluN1, and SV2A protein levels in DIV14 Syngap1+/ls mouse cortical neurons^[2].
In Syngap1^+/- mouse neurons, SR-1815 (1.5 µM; 14 d) increases dendritic spine size and dendritic/MAP2 development, and elevates SynGAP, PSD-95, and GluN1^[4].

SR-1815 (1.5 μM; 14 days) doubles SynGAP protein in cortical neurons of Syngap1^+/- mice^[1].
SR-1815 is a relatively selective multikinase binder in the KINOMEscan panel, with strong binding activity against CLK1/2^[2].
SR-1815 (10 µM; 24-48 h) reduces pan-phosphorylated SR protein signals in pc293T cells at 24 and 48 h^[2].
SR-1815 (2 weeks) extensively remodels the transcriptome and proteome of mouse cortical neurons, with 452 overlapping RNA/protein changes after 2 weeks^[2].
SR-1815 upregulates SynGAP expression in neurons of Syngap1 haploinsufficiency mice^[2].
SR-1815 increases endogenous SynGAP and reduces synaptic and circuit hyperexcitability in primary mouse cortical neurons with Syngap1 haploinsufficiency^[3].
SR-1815 induces consistent changes at the transcript and protein levels, consistent with the regulation of gene expression levels^[3].
SR-1815 is a multikinase inhibitor that controls neuronal SynGAP abundance by inhibiting the CLK family and reducing toxic exon inclusion^[3].
In cell-free kinase assays, SR-1815 directly inhibits CLK1 and CLK2 with IC₅₀ values of 446 nM and 605 nM, respectively, and more weakly inhibits CLK3 with 6.8 µM^[4].
In pc293T cells, SR-1815 (10 µM; 48 h) remodels chromatin occupancy, recruits CLK1/3/4 and splicing factors, while displacing CLK2 and CaMKII^[4].
In cortical neurons, SR-1815 (4 h-2 weeks) induces time-dependent transcriptomic and proteomic changes, enriched in synaptic, cytoskeletal, and mRNA processing programs^[4].