ErSO-TFPy (72 hours) effectively inhibited the viability of ERα-positive human breast cancer cell lines, with an IC50 value of approximately 5-25 nM after 72 hours of incubation, while its activity against ERα-negative human breast cancer cell lines was extremely low [2]. ErSO-TFPy (150-450 nM; 6 hours) activated the expected unfolded protein response in MCF-7 human breast cancer cells after incubation at concentrations of 150 nM and 450 nM for 6 hours, manifested as increased phosphorylation levels of EIF2α, increased phosphorylation levels of AMPK, and cleavage of ATF6 [2]. ErSO-TFPy (≥0.01 μM; 72 h) induced potent TRPM4-dependent cell death in MCF-7 human breast cancer cells, with a cell death rate of approximately 80% after 72 hours of incubation at a concentration of ≥0.01 μM, while MCF-7 TRPM4 knockout cells showed a 1000-fold decrease in sensitivity to ErSO-TFPy-induced cell death [2]. ErSO-TFPy (1 μM; 2 h) induced significant TRPM4-dependent cell swelling in MCF-7 parental human breast cancer cells after 2 hours of incubation at a concentration of 1 μM, while no measurable cell swelling was observed in MCF-7 TRPM4 knockout cells [2]. ErSO-TFPy (24-120 hours) can effectively inhibit the activity of human breast cancer cells of MCF-7, MCF-7Y537S mutant and MCF-7D538G mutant. After incubation in 10% FBS and 10% CD-FBS + 1 nME2 medium for 24 hours and 120 hours, the IC50 values were in the single digit nanomolar range [2].

ErSO-TFPy (TEQ103) (total dose 1-150 mg/kg; intravenous injection) showed significant and durable antitumor activity in athymic female mice carrying MCF-7 tumors, achieving 100% tumor clearance regardless of the dosing regimen [1]. ErSO-TFPy (2-10 mg/kg; intravenous injection; once a week; for a total of 4 times) completely regressed MCF-7 ERα+ breast cancer xenografts in athymic nude mice at a dose of 10 mg/kg, significantly inhibited tumor growth at a dose of 5 mg/kg, and had no significant inhibitory effect at a dose of 2 mg/kg, with no significant weight loss [2]. ErSO-TFPy (20 mg/kg; intravenous injection; once or twice a week; for a total of 4 times) completely regressed ST941 ESR1mut breast cancer PDX tumors resistant to fulvestrant in athymic nude mice [2]. ErSO-TFPy (2-50 mg/kg; intravenous injection; single dose) in athymic nude mice at doses of 25 mg/kg or 50 mg/kg caused almost complete or complete regression of MCF-7 ESR1D538G breast cancer xenografts (including large tumors with a volume of approximately 1500 mm³), with significant inhibitory effect at a dose of 5 mg/kg and no significant inhibitory effect at a dose of 2 mg/kg [2]. ErSO-TFPy (50 mg/kg; intravenous injection; single dose) in athymic nude mice caused significant regression of BT-474 ERα+/HER2+ breast cancer xenografts (including large tumors that had already formed) [2]. ErSO-TFPy (50 mg/kg; intravenous injection; single dose) can induce rapid necrotizing cell death in MCF-7 ESR1D538G breast cancer xenografts. More than 90% of the tumors were observed to die within 3 to 5 days after treatment, and no significant early involvement of tumor cell death was found in the assessed immune cell population [2].

Western Blot Analysis [2]
Cell Types: MCF-7 human breast cancer cells
Tested Concentrations: 150 nM, 450 nM
Incubation Duration: 6 hours
Experimental Results: Activation of expected unfolded protein response markers was induced, including phosphorylation of EIF2α, phosphorylation of AMPK and cleavage of ATF6.

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Cell viability assay [2]
Cell Types: MCF-7 parental cells and MCF-7 TRPM4 KO human breast cancer cells
Tested Concentrations: ≥0.01 μM (MCF-7 parental cells; 72 hours); 100 μM (MCF-7 TRPM4 KO cells; 168 hours)
Incubation Duration: 24 hours, 72 hours, 168 hours
Experimental Results: At a concentration of ≥0.01 μM, the mortality rate of MCF-7 parental cells was approximately 80% after 72 hours. In MCF-7 TRPM4 KO cells, the cell death rate was reduced by approximately 1000-fold, and very few cell deaths were observed even after incubation at a concentration of 100 μM for 168 hours.

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Cell viability assay [2]
Cell Types: MCF-7, MCF-7 Y537S mutant and MCF-7 D538G mutant human breast cancer cells
Tested Concentrations: 4-8 nM (24 hours); 4-8 nM (120 hours)
Incubation Duration: 24 hours, 120 hours
Experimental Results: In 10% FBS medium, the IC50 values of MCF-7 cells reached single digit nanomolar levels: 8 nM (24 hours), 5 nM (120 hours); the IC50 values of MCF-7 Y537S cells reached 5 nM (24 hours), 4 nM (120 hours); in MCF-7 D538G cells, the IC50 values were 6 nM (24 h) and 6 nM, respectively. (120 h). In 10% CD-FBS + 1 nM E2 medium, the IC50 values reached single-digit nanomolar levels: 7 nM (24 h) and 6 nM (120 h) in MCF-7 cells; 4 ± 1 nM (24 h) and 6 nM (120 h) in MCF-7 Y537S cells; and 5 nM (24 h) and 8 nM (120 h) in MCF-7 D538G cells.

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Cytotoxicity assay [2]
Cell Types: MCF-7 human breast cancer cells
Tested Concentrations: 50 nM
Incubation Duration: 24 hours, 120 hours
Experimental Results: Incubation at 50 nM for 24 hours induced approximately 80% cell death. Incubation at 50 nM for 120 hours induced approximately 80% cell death.

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Animal/Disease Models:Athymic (female; subcutaneously carrying approximately 500 mm3 MCF-7 tumors) [1]
Doses: 1 mg/kg, 2 mg/kg, 4 mg/kg, 15 mg/kg, 30 mg/kg; 1 mg/kg, 5 mg/kg, 20 mg/kg, 75 mg/kg, 150 mg/kg (intermittent dosing regimen, day 1 and day 10)
Route of Administration: Intravenous injection; once daily for 10 consecutive days (daily dosing regimen); intravenous injection; single dosing on day 1 and day 10 (intermittent dosing regimen)
Experimental Results: The 2 mg/kg daily dosing regimen resulted in 2 out of 9 mice surviving without tumors, and tumor growth was delayed by 44 days in relapsed mice. The 5 mg/kg intermittent dosing regimen resulted in 4 out of 9 relapsed mice surviving with complete tumor regression, and tumor growth was delayed by 56 days. At both dosing regimens, with a total dose ≥40 mg/kg, all mice survived and their tumors completely regressed for up to 121 days. No weight loss was observed across all study dose ranges.

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Animal/Disease Models:Athymic nude mice (female, implanted with exogenous estradiol sustained-release tablets) [2]
Doses: 2 mg/kg; 5 mg/kg; 10 mg/kg
Route of Administration: Intravenous injection; once a week; for a total of 4 times
Experimental Results: The 2 mg/kg dose group did not show significant tumor growth inhibition compared with the solvent control group. The 5 mg/kg dose group induced significant tumor growth inhibition. The 10 mg/kg dose group induced complete tumor regression. No significant weight loss was caused in any of the treatment groups.

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Animal/Disease Models:Athymic nude mice [2]
Doses: 20 mg/kg
Route of Administration: Intravenous injection; once a week; 4 times; Intravenous injection; twice a week; 4 times
Experimental Results: Both administration regimens resulted in complete tumor regression in all 8 mice. Compared with the solvent group, both administration regimens significantly reduced tumor volume.

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Animal/Disease Models:Athymic nude mice (female) [2]
Doses: 2 mg/kg; 5 mg/kg; 25 mg/kg; 50 mg/kg
Route of Administration: Intravenous injection; single dose (day 0); intravenous injection; single dose (day 53)
Experimental Results: No significant tumor growth inhibition was observed in the 2 mg/kg dose group. Significant tumor growth inhibition was induced in the 5 mg/kg dose group. More than 80% tumor volume reduction was induced in the 25 mg/kg and 50 mg/kg dose groups within 14 days. No measurable tumors were detected in any of the 50 mg/kg dose group at day 66. More than 90% tumor regression was induced in tumors of approximately 1500 mm3 at day 53.

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Animal/Disease Models:Athymic nude mice (implanted with 0.5 mg 90-day sustained-release estrogen granules) [2]
Doses: 50 mg/kg
Route of Administration: Intravenous injection; single dose (day 0); intravenous injection; single dose (day 28)
Experimental Results: On day 0, the tumor volume shrank by more than 80% within 14 days, and the tumor continued to regress until day 35. On day 28, large tumors regressed significantly.

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Animal/Disease Models:Athymic nude mice (female) [2]
Doses: 50 mg/kg
Route of Administration: Intravenous injection; single dose
Experimental Results: Tumor regression was induced on day 1 post-treatment. More than 90% of tumor tissue necrosis was achieved on days 3 and 5 post-treatment. Compared with the control group, Ki67+ proliferating cells and cleaved caspase-3+ apoptotic cells were significantly reduced in tumor tissue on day 1 post-treatment. Compared with the control group, there was no significant difference in the number of Ly6G+ neutrophils, CD11c+ dendritic cells, or F4/80+ macrophages in surviving tumor areas.

[1]. Abstract 5629_ TEQ103, a novel therapeutic for the treatment of estrogen receptor alpha positive (ERα+) breast cancer. Cancer Res (2025) 85 (8_Supplement_1): 5629.

[2]. Single Dose of a Small Molecule Leads to Complete Regressions of Large Breast Tumors in Mice. ACS Cent Sci. 2025;11(2):228-238. Published 2025 Jan 22.

C19H13F7N2O2

434.31

3035547-78-2

White to off-white solid

O=C1[C@@](N2CC(F)(C(F)(C2)F)F)(C3=CC=C(C=C3)O)C4=CC=CC(C(F)(F)F)=C4N1

TEQ103; Sera2

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~230.25 mM; with sonication)

Solubility in Formulation 1: ≥ 5 mg/mL (11.51 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (50.0 mg/mL) to 400 μL of PEG300 and mix well; then add 50 μL of Tween-80 and mix well; finally add 450 μL of physiological saline and adjust the volume to 1 mL. Preparation of physiological saline: Dissolve 0.9 g of sodium chloride in double-distilled water and dilute to 100 mL to obtain clear physiological saline.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 5 mg/mL (11.51 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (50.0 mg/mL) to 900 μL of 20% SBE-β-CD saline and mix well. Preparation of 20% SBE-β-CD saline (4°C, store for one week): Dissolve 2 g of SBE-β-CD powder in 10 mL of saline until completely dissolved and clear.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 5 mg/mL (11.51 mM)(saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (50.0 mg/mL) to 900 μL of corn oil and mix well.

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 (Please use freshly prepared in vivo formulations for optimal results.)