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ht1197 (ATCC)

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ATCC ht1197
Ht1197, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 223 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ht1197/product/ATCC
Average 95 stars, based on 223 article reviews

ht1197 - by Bioz Stars, 2026-03

95/100 stars

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Amiodarone decreases proliferation in bladder cancer cell lines. Real-time proliferation assays in UMUC3, HT1197, BFTC905, and RT112 were conducted using the Incucyte S3 system. The cells were treated with increasing concentrations of amiodarone (0–50 μmol/L), and the confluence was measured every 4 hours over 96 hours. A, Cell confluence over time. B, Cell confluence after 96 hours of treatment. Data represent mean ± SEM from at least three independent experiments (one-way ANOVA with Dunnett’s multiple comparisons test; *, P < 0.05; ***, P < 0.001; ****, P < 0.0001). C, Concentration–response curves and IC 50 values for amiodarone after 96 hours of treatment.

Journal: Cancer Research Communications

Article Title: Repurposing Amiodarone for Bladder Cancer Treatment

doi: 10.1158/2767-9764.CRC-24-0433

Figure Lengend Snippet: Amiodarone decreases proliferation in bladder cancer cell lines. Real-time proliferation assays in UMUC3, HT1197, BFTC905, and RT112 were conducted using the Incucyte S3 system. The cells were treated with increasing concentrations of amiodarone (0–50 μmol/L), and the confluence was measured every 4 hours over 96 hours. A, Cell confluence over time. B, Cell confluence after 96 hours of treatment. Data represent mean ± SEM from at least three independent experiments (one-way ANOVA with Dunnett’s multiple comparisons test; *, P < 0.05; ***, P < 0.001; ****, P < 0.0001). C, Concentration–response curves and IC 50 values for amiodarone after 96 hours of treatment.

Article Snippet: UMUC3 (basal mesenchymal phenotype) was obtained from Sigma-Aldrich, HT1197 (G4) from ATCC (CRL1473), and BFTC905 (G3) and RT112 (G2) from the German Collection of Microorganisms and Cell Cultures GmbH.

Techniques: Concentration Assay

Amiodarone induces apoptosis in bladder cancer cell lines. Cells were treated for 48 or 72 hours with amiodarone (0, 25, and 50 μmol/L for UMUC3; 0, 12.5, and 25 μmol/L for HT1197, BFTC905, and RT112). A, Apoptosis was evaluated using the Caspase-Glo 3/7 Assay and viability using the CellTiter cell proliferation assay. Apoptosis results were normalized to viability. Data are presented as apoptosis related to the control and represent mean ± SEM from at least three independent experiments (one-way ANOVA with Dunnett’s multiple comparisons test; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001). B, Western blot analysis of cPARP expression after 48 hours of treatment with 0, 12.5, and 25 μmol/L amiodarone. GAPDH was used as a loading control. Blots are representative of three independent experiments. Quantification of cPARP expression (normalized by GAPDH) is indicated under each corresponding band. Values are presented as expression related to the control.

Journal: Cancer Research Communications

Article Title: Repurposing Amiodarone for Bladder Cancer Treatment

doi: 10.1158/2767-9764.CRC-24-0433

Figure Lengend Snippet: Amiodarone induces apoptosis in bladder cancer cell lines. Cells were treated for 48 or 72 hours with amiodarone (0, 25, and 50 μmol/L for UMUC3; 0, 12.5, and 25 μmol/L for HT1197, BFTC905, and RT112). A, Apoptosis was evaluated using the Caspase-Glo 3/7 Assay and viability using the CellTiter cell proliferation assay. Apoptosis results were normalized to viability. Data are presented as apoptosis related to the control and represent mean ± SEM from at least three independent experiments (one-way ANOVA with Dunnett’s multiple comparisons test; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001). B, Western blot analysis of cPARP expression after 48 hours of treatment with 0, 12.5, and 25 μmol/L amiodarone. GAPDH was used as a loading control. Blots are representative of three independent experiments. Quantification of cPARP expression (normalized by GAPDH) is indicated under each corresponding band. Values are presented as expression related to the control.

Techniques: Caspase-Glo Assay, Proliferation Assay, Control, Western Blot, Expressing

(a) Overview of medicinal chemistry strategy for covalent PPARG inverse agonist optimization resulting in FTX-6746. (b) Crystal structure of FTX-6746 covalent adduct with PPARG LBD. The PPARG LBD (gray) adopts a similar conformation to that observed with T0070907 (PDB 6ONI) with H12 (orange) inserted into the ligand binding pocket with the C-terminal carboxylate forming a key H-bond with the quinolone nitrogen of the FTX-6746 adduct (yellow dashes). (c) Dose-dependent recruitment of NCOR1 ID2 to RXRA S427F :PPARG heterodimers, demonstrating the superiority of FTX-6746 for countering the activation bias driven by this mutation over T0070907 and SR10221. Representative curves from ≥ 3 biological replicates are shown. Data points indicate the average of technical duplicates from a representative biological replicate. The 95% confidence interval for EC 50 values of SR10221, T0070907 and FTX-6746, respectively, were determined to be: 109 nM ± 30 nM, 60.5 ± nM, 197.5 ± 8.5 nM. The 95% confidence interval for the E max values relative to T0070907 for SR10221 and FTX- 6746, respectively, were determined to be: 6.2 ± 0.6% and 170.5 ± 2%. Rosiglitazone was not present for these experiments. (d) Comparison of SR10221, T007097 and FTX-6746 ability to suppress PPARG target gene ANGPTL4 in RXRA WT (blue, 5637 cell line) and RXRA S427F (orange, HT1197 cell line) contexts. Data indicate the activation bias observed biochemically reduces T0070907 and SR10221 efficacy and the superior repressive biasing of FTX-6746 enables it to achieve similar repressive effects in both contexts. Data is representative of two separate biological experiments.

Journal: bioRxiv

Article Title: Discovery and characterization of FX-909, a covalent inverse agonist of PPARG rationally designed to impose a powerful repressive bias in PPARG for the treatment of PPARG/RXRA-activated muscle-invasive urothelial cancers

doi: 10.1101/2025.05.08.652848

Figure Lengend Snippet: (a) Overview of medicinal chemistry strategy for covalent PPARG inverse agonist optimization resulting in FTX-6746. (b) Crystal structure of FTX-6746 covalent adduct with PPARG LBD. The PPARG LBD (gray) adopts a similar conformation to that observed with T0070907 (PDB 6ONI) with H12 (orange) inserted into the ligand binding pocket with the C-terminal carboxylate forming a key H-bond with the quinolone nitrogen of the FTX-6746 adduct (yellow dashes). (c) Dose-dependent recruitment of NCOR1 ID2 to RXRA S427F :PPARG heterodimers, demonstrating the superiority of FTX-6746 for countering the activation bias driven by this mutation over T0070907 and SR10221. Representative curves from ≥ 3 biological replicates are shown. Data points indicate the average of technical duplicates from a representative biological replicate. The 95% confidence interval for EC 50 values of SR10221, T0070907 and FTX-6746, respectively, were determined to be: 109 nM ± 30 nM, 60.5 ± nM, 197.5 ± 8.5 nM. The 95% confidence interval for the E max values relative to T0070907 for SR10221 and FTX- 6746, respectively, were determined to be: 6.2 ± 0.6% and 170.5 ± 2%. Rosiglitazone was not present for these experiments. (d) Comparison of SR10221, T007097 and FTX-6746 ability to suppress PPARG target gene ANGPTL4 in RXRA WT (blue, 5637 cell line) and RXRA S427F (orange, HT1197 cell line) contexts. Data indicate the activation bias observed biochemically reduces T0070907 and SR10221 efficacy and the superior repressive biasing of FTX-6746 enables it to achieve similar repressive effects in both contexts. Data is representative of two separate biological experiments.