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Synta Inc synta66
Synta66, supplied by Synta Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/synta66/us12655113-85-0-10
Average 86 stars, based on 1 article reviews
synta66 - by Bioz Stars, 2026-09
86/100 stars

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Related Articles

Gene Expression:

Article Title: CRAC channels drive digital activation and provide analog control and synergy to Ca(2+)-dependent gene regulation.
Article Snippet: GFP expression was inhibited following pretreatmentwith either the calcineurin blocker cyclosporin A (Figure 1B) or the CRAC channel blocker Synta66 ([11]; Figure 1C, labeled Synta then Thap). .. Application *Correspondence: anant.parekh@dpag.ox.ac.uk of Synta66 just 10 min after thapsigargin exposure brought cytoplasmicCa2+ back to resting levels within 4min (Figure 1H) but failed to reduce subsequent gene expression (Figure 1C, labeled Thap then Synta). ..

Labeling:

Article Title: CRAC channels drive digital activation and provide analog control and synergy to Ca(2+)-dependent gene regulation.
Article Snippet: GFP expression was inhibited following pretreatmentwith either the calcineurin blocker cyclosporin A (Figure 1B) or the CRAC channel blocker Synta66 ([11]; Figure 1C, labeled Synta then Thap). .. Application *Correspondence: anant.parekh@dpag.ox.ac.uk of Synta66 just 10 min after thapsigargin exposure brought cytoplasmicCa2+ back to resting levels within 4min (Figure 1H) but failed to reduce subsequent gene expression (Figure 1C, labeled Thap then Synta). ..

Multiple Displacement Amplification:

Article Title: Store-Operated Ca 2+ Entry in Tumor Progression: From Molecular Mechanisms to Clinical Implications
Article Snippet: .. A recent study reported that Synta66, a relatively new potent and selective SOCE blocker developed by Synta Pharmaceuticals [ ], impaired the migratory and proliferative capabilities of MDA-MB-468 triple-negative breast cancer cells in response to EGF stimulation [ ]. ..

Binding Assay:

Article Title: A CNA-35-based high-throughput fibrosis assay reveals ORAI1 as a regulator of collagen release from pancreatic stellate cells.
Article Snippet: .. To ensure proper binding of Synta66 to ORAI1 channels, PS-1 cells were preincubated with 10 μM Synta-66, or in case of control, with 0.1 % DMSO. .. Then, cells were superfused with Ca2+-free, 1 mM Mn2+-supplemented Ringer’s solution with 284 μM vitamin C, 10 μM Synta-66 or 0.1 % DMSO.

Control:

Article Title: A CNA-35-based high-throughput fibrosis assay reveals ORAI1 as a regulator of collagen release from pancreatic stellate cells.
Article Snippet: .. To ensure proper binding of Synta66 to ORAI1 channels, PS-1 cells were preincubated with 10 μM Synta-66, or in case of control, with 0.1 % DMSO. .. Then, cells were superfused with Ca2+-free, 1 mM Mn2+-supplemented Ringer’s solution with 284 μM vitamin C, 10 μM Synta-66 or 0.1 % DMSO.

other:

Article Title: Biphenyl compounds as SOCE modulators, compositions and uses thereof
Article Snippet: Synta66 (GSK1349571A; 3-fluoropyridine-4-carboxylic acid (2′,5′-dimethoxybiphenyl-4-yl)amide) is a compound developed by Synta Pharmaceuticals and GSK.

Article Title: Molecular pharmacology of store-operated CRAC channels
Article Snippet: Recently, a new compound called Synta66 (3-fluoropyridine-4-carboxylic acid (2′,5′-dimethoxybiphenyl-4-yl)amide), developed by Synta pharmaceuticals, has gained significant attention for its ability to selectively inhibit CRAC channels.

Article Title: A CNA-35-based high-throughput fibrosis assay reveals ORAI1 as a regulator of collagen release from pancreatic stellate cells.
Article Snippet: In contrast, the collagen release from NIH-3T3 cells is not affected by 10 μM Synta-66.

Article Title: Orai inhibition modulates pulmonary ILC2 metabolism and alleviates airway hyperreactivity in murine and humanized models
Article Snippet: In a future study, it might be interesting to compare Synta66 with compound 5D, because Synta shows some selectivity to Orai1 over Orai2 and 3.



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Pharmacological inhibition of SOCE suppresses IFN-γ–induced PD-L1 expression in OSCC cells. (A) HSC-3 cells were pretreated with the SOCE inhibitor <t>Synta66</t> (1–20 μM) and stimulated with IFN-γ (100 ng/mL, 6 h). PD-L1 and GAPDH protein levels were analyzed by Western blot. PD-L1 is detected as multiple bands, which most likely reflect heterogeneous N-linked glycosylation and maturation states of the protein. (B) PD-L1 expression was examined in cells treated with Synta66 (20 μM) alone under unstimulated conditions. (C) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 3 h). PD-L1 mRNA was assessed by RT-qPCR. (D) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 6 h). PD-L1 protein levels were analyzed by Western blot. Quantitative data are shown as mean ± SEM from four independent biological replicates (n = 4). Exact p-values or significance levels (p < 0.001 or ns) are indicated in the figure. Representative Western blot images are shown.
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Pharmacological inhibition of SOCE suppresses IFN-γ–induced PD-L1 expression in OSCC cells. (A) HSC-3 cells were pretreated with the SOCE inhibitor <t>Synta66</t> (1–20 μM) and stimulated with IFN-γ (100 ng/mL, 6 h). PD-L1 and GAPDH protein levels were analyzed by Western blot. PD-L1 is detected as multiple bands, which most likely reflect heterogeneous N-linked glycosylation and maturation states of the protein. (B) PD-L1 expression was examined in cells treated with Synta66 (20 μM) alone under unstimulated conditions. (C) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 3 h). PD-L1 mRNA was assessed by RT-qPCR. (D) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 6 h). PD-L1 protein levels were analyzed by Western blot. Quantitative data are shown as mean ± SEM from four independent biological replicates (n = 4). Exact p-values or significance levels (p < 0.001 or ns) are indicated in the figure. Representative Western blot images are shown.
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Global Ca 2+ signaling was analyzed in Jurkat WT T cells ( A ) and Jurkat Hn1l/Jpt2 -/- T cells ( B ), loaded with Fura2-AM. MASTER-NAADP (100 nM), MASTER-NADP (100 nM), or NAADP-AM (100 nM) were added as indicated. Experiments were carried out at 37 °C and SOCE was blocked by pre-incubation of 50 µM <t>Synta66</t> for 5 min prior to imaging. Number of cells indicated in figure. Aggregated data are mean amplitude per peak ( C ), mean number of Ca 2+ peaks ( D ), percentage of responding cells ( E ), and calculation of the mean responsiveness (number of peaks * amplitude; F presented as mean ± SEM; Jurkat WT MASTER-NAADP, n = 240 cells; Jurkat WT MASTER-NADP, n = 120 cells; Jurkat WT NAADP-AM, n = 91 cells; Jurkat Hn1l/Jpt2 -/- MASTER-NAADP, n = 181 cells; Jurkat Hn1l/Jpt2 -/- MASTER-NADP, n = 113 cells; Jurkat Hn1l/Jpt2 -/- NAADP-AM, n = 110 cells. Nonparametric Kruskal-Wallis test and Dunn’s correction for multiple testing * P < 0.05; **** P < 0.0001. Source data and exact p values are provided as a Source Data file.
Synta66, supplied by Merck & Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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Image Search Results


Pharmacological inhibition of SOCE suppresses IFN-γ–induced PD-L1 expression in OSCC cells. (A) HSC-3 cells were pretreated with the SOCE inhibitor Synta66 (1–20 μM) and stimulated with IFN-γ (100 ng/mL, 6 h). PD-L1 and GAPDH protein levels were analyzed by Western blot. PD-L1 is detected as multiple bands, which most likely reflect heterogeneous N-linked glycosylation and maturation states of the protein. (B) PD-L1 expression was examined in cells treated with Synta66 (20 μM) alone under unstimulated conditions. (C) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 3 h). PD-L1 mRNA was assessed by RT-qPCR. (D) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 6 h). PD-L1 protein levels were analyzed by Western blot. Quantitative data are shown as mean ± SEM from four independent biological replicates (n = 4). Exact p-values or significance levels (p < 0.001 or ns) are indicated in the figure. Representative Western blot images are shown.

Journal: The Journal of Physiological Sciences : JPS

Article Title: Orai1- and STIM1-mediated calcium signaling controls PD-L1 expression and modulates antitumor immunity in oral cancer

doi: 10.1016/j.jphyss.2026.100063

Figure Lengend Snippet: Pharmacological inhibition of SOCE suppresses IFN-γ–induced PD-L1 expression in OSCC cells. (A) HSC-3 cells were pretreated with the SOCE inhibitor Synta66 (1–20 μM) and stimulated with IFN-γ (100 ng/mL, 6 h). PD-L1 and GAPDH protein levels were analyzed by Western blot. PD-L1 is detected as multiple bands, which most likely reflect heterogeneous N-linked glycosylation and maturation states of the protein. (B) PD-L1 expression was examined in cells treated with Synta66 (20 μM) alone under unstimulated conditions. (C) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 3 h). PD-L1 mRNA was assessed by RT-qPCR. (D) Cells were pretreated with Synta66 (20 μM, 3 h), followed by IFN-γ (100 ng/mL, 6 h). PD-L1 protein levels were analyzed by Western blot. Quantitative data are shown as mean ± SEM from four independent biological replicates (n = 4). Exact p-values or significance levels (p < 0.001 or ns) are indicated in the figure. Representative Western blot images are shown.

Article Snippet: The SOCE channel inhibitor Synta66, which targets Orai1 forming the pore of the CRAC channel, was purchased from MedChemExpress (Monmouth Junction, NJ, USA), respectively.

Techniques: Inhibition, Expressing, Western Blot, Glycoproteomics, Quantitative RT-PCR

Global Ca 2+ signaling was analyzed in Jurkat WT T cells ( A ) and Jurkat Hn1l/Jpt2 -/- T cells ( B ), loaded with Fura2-AM. MASTER-NAADP (100 nM), MASTER-NADP (100 nM), or NAADP-AM (100 nM) were added as indicated. Experiments were carried out at 37 °C and SOCE was blocked by pre-incubation of 50 µM Synta66 for 5 min prior to imaging. Number of cells indicated in figure. Aggregated data are mean amplitude per peak ( C ), mean number of Ca 2+ peaks ( D ), percentage of responding cells ( E ), and calculation of the mean responsiveness (number of peaks * amplitude; F presented as mean ± SEM; Jurkat WT MASTER-NAADP, n = 240 cells; Jurkat WT MASTER-NADP, n = 120 cells; Jurkat WT NAADP-AM, n = 91 cells; Jurkat Hn1l/Jpt2 -/- MASTER-NAADP, n = 181 cells; Jurkat Hn1l/Jpt2 -/- MASTER-NADP, n = 113 cells; Jurkat Hn1l/Jpt2 -/- NAADP-AM, n = 110 cells. Nonparametric Kruskal-Wallis test and Dunn’s correction for multiple testing * P < 0.05; **** P < 0.0001. Source data and exact p values are provided as a Source Data file.

Journal: Nature Communications

Article Title: MASTER-NAADP: a membrane permeable precursor of the Ca 2+ mobilizing second messenger NAADP

doi: 10.1038/s41467-024-52024-y

Figure Lengend Snippet: Global Ca 2+ signaling was analyzed in Jurkat WT T cells ( A ) and Jurkat Hn1l/Jpt2 -/- T cells ( B ), loaded with Fura2-AM. MASTER-NAADP (100 nM), MASTER-NADP (100 nM), or NAADP-AM (100 nM) were added as indicated. Experiments were carried out at 37 °C and SOCE was blocked by pre-incubation of 50 µM Synta66 for 5 min prior to imaging. Number of cells indicated in figure. Aggregated data are mean amplitude per peak ( C ), mean number of Ca 2+ peaks ( D ), percentage of responding cells ( E ), and calculation of the mean responsiveness (number of peaks * amplitude; F presented as mean ± SEM; Jurkat WT MASTER-NAADP, n = 240 cells; Jurkat WT MASTER-NADP, n = 120 cells; Jurkat WT NAADP-AM, n = 91 cells; Jurkat Hn1l/Jpt2 -/- MASTER-NAADP, n = 181 cells; Jurkat Hn1l/Jpt2 -/- MASTER-NADP, n = 113 cells; Jurkat Hn1l/Jpt2 -/- NAADP-AM, n = 110 cells. Nonparametric Kruskal-Wallis test and Dunn’s correction for multiple testing * P < 0.05; **** P < 0.0001. Source data and exact p values are provided as a Source Data file.

Article Snippet: Additionally, Jurkat T cells were incubated with 50 µM Synta66 (Merck) for 5 min prior to imaging to block SOCE through inhibition of Orai1.

Techniques: Incubation, Imaging