BY13 (0.1-10 μM, 24 hours) reduced the levels of SRC-3 and ERα proteins in MCF-7 cells in a dose-dependent manner, degrading them by 71% and 85%, respectively [1]. BY13 (0.01-10 μM, 36 hours) effectively inhibited the proliferation of wild-type, mutant and drug-resistant breast cancer cells (IC50 of 0.003-0.35 μM for MCF-7, LCC2 and MCF-7D538G/Y537S/EGFR cells), and degraded SRC-3 and ERα in mutant cells in a dose-dependent manner (especially at a concentration of 0.1 μM, the degradation effect on MCF-7Y537S cells was more significant) [1]. BY13 (0.1-10 μM, 3-48 hours) effectively reduced the protein levels of SRC-3 and ERα, with better effects than fulvestrant, and reached maximum degradation after 36 hours, after which it hardly increased over time in LCC2 cells [1]. BY13 (0.01-20 μM, 36 hours) significantly reduced the protein levels of SRC-3 (0.1 μM only) and ERα (1 μM only) in MCF-7 cells (the half-lethal concentration of SRC-3 was 0.031 μM), and was subtype selective, with stronger inhibitory effects on SRC-1 than on SRC-2 [1]. BY13 (0.01-5 μM, 24 hours) downregulated the protein level of AR in MCF-7 cells, but its effect was weaker than that on ERα, and it had a moderate inhibitory effect on AR-overexpressing LNCaP cells (IC50: 1.43 μM) [1]. BY13 (1 μM, 36 h) significantly reduced the level of SRC-3 protein in MCF-7 cells via the ubiquitin-proteasome system (UPS) pathway (a similar phenomenon was observed in LCC2 cells) [1]. BY13 (1 μM, 6 h, 40-76°C) can enter tumor cells and bind directly to SRC-3, significantly enhancing the thermal stability of SRC-3 protein in MCF-7 cells at high temperatures [1]. BY13 (10 μM, 6 h) induces spatial proximity between SRC-3 and CRBN, thereby promoting the formation of the SRC-3-BY13-CRBN ternary complex in MCF-7 cells [1]. BY13 (0.01-10 μM, 36 h) significantly increased the mRNA expression level of SRC-3 in LCC2 cells with increasing concentration and effectively reduced the mRNA level of ERα [1]. BY13 (1-20 μM, 48 h) significantly induced apoptosis in breast cancer cells and enhanced early and late apoptosis in MCF-7 and LCC2 cells. BY13 (5-20 μM, 48 hours) dose-dependently arrested LCC2 cells in the G1 phase, with a significantly higher proportion of cells in the G1 phase than in the S phase. BY13 (0.01-100 μM) exhibited good metabolic stability and acceptable safety, with IC50 values of 2.73 μM for CYP3A4 and 1.1 μM for hERG channels.

BY13 (3-10 μM/kg, intraperitoneal injection, once every two days for 23 days) has strong anti-endocrine resistance activity by targeting SRC-3 and ERα degradation, has high safety, and can improve the poor prognosis of endocrine resistant breast cancer in LCC2 xenograft mouse model [1].

Western Blot Analysis [1]
Cell Types: MCF-7 cells, LCC2 cells
Tested Concentrations: 0.01, 0.1, 1, 5, 10 μM
Incubation Duration: 24 hours
Experimental Results: At a concentration of 1 μM, both SRC-3 and ERα proteins in MCF-7 cells were degraded, with degradation rates of 71% and 85%, respectively. In MCF-7 cells, the levels of SRC-3 and ERα proteins decreased in a dose-dependent manner, and no typical "hook effect" was observed. In LCC2 cells, the degradation rates of SRC-3 and ERα proteins were significantly higher than those of fulvestrant. In MCF-7 cells, the level of AR protein was also downregulated, but its downregulation effect was weaker than that of ERα.

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Western Blot Analysis [1]
Cell Types: MCF-7 cells, LCC2 cells
Tested Concentrations: 1 μM
Incubation Duration: MCF-7 cells (3, 6, 9, 12, 24, 36 hours), LCC2 cells (3, 6, 9, 12, 24, 36, 48 hours)
Experimental Results: After 24 hours, the SRC-3 protein level in MCF-7 cells decreased significantly, reaching maximum degradation after 36 hours. The SRC-3 protein level in LCC2 cells decreased significantly after 9 hours of treatment, reaching maximum degradation after 36 hours, and degradation hardly increased further.

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Western Blot Analysis [1]
Cell Types: MCF-7 cells, LCC2 cells
Tested Concentrations: 1 μM, after 2 hours of treatment with 1 μM MG-132, bortezomib, chloroquine, or (BY13-Neg, SI-2, and pomalidomide)
Incubation Duration: 36 hours
Experimental Results: SRC-3 protein levels were significantly reduced, dependent on the ubiquitin-proteasome system (UPS) pathway, but this effect could be reversed by two proteasome inhibitors (MG-132, bortezomib, and SI-2), while BY13-Neg could not (similar symptoms were observed in LCC2 cells).

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Apoptosis Analysis [1]
Cell Types: MCF-7 cells, LCC2 cells
Tested Concentrations: 1, 5, 10, 20 μM
Incubation Duration: 48 hours
Experimental Results: In MCF-7 cells, increasing concentration effectively induced apoptosis and enhanced early and late apoptosis (early apoptosis rate up to 35%). In LCC2 cells, 1 μM mainly induced late apoptosis, 10 μM induced early apoptosis, and 20 μM induced strong early apoptosis (early apoptosis rate > 30%).

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Animal/Disease Models:LCC2 cells (5 × 10⁶ cells/mouse) were subcutaneously injected into the right axilla of 4-week-old female Balb/c nude mice to establish an LCC2 xenograft mouse model [1].
Doses: 3, 5, 10 μM/kg, tamoxifen (10 μM/kg) and fulvestrant (5 μM/kg)
Route of Administration: Intraperitoneal injection, once every two days for 23 days until the tumor volume reached about 100 mm³, and then samples were collected on day 36.
Experimental Results: The 3 μM/kg dose group significantly inhibited tumor growth, and the 5 μM/kg dose group had a better effect, with a tumor growth inhibition rate of 54%. At the 3 μM/kg dose, SRC-3 protein in the tumor tissue was almost completely degraded; at the 5 μM/kg dose, the protein levels of SRC-3 and ERα were further reduced. This drug exhibits a wide therapeutic window, and no significant increase in body weight was observed in mouse models at doses up to 10 μM/kg. No significant histopathological changes were observed in mouse model organs and tissues during administration at 3 μM/kg and 5 μM/kg, demonstrating good safety. At doses of 3 μM/kg and 5 μM/kg, the drug reduced Ki-67 expression levels in tumor tissues, thereby improving the poor prognosis of endocrine-resistant breast cancer.

[1]. Intercepting the Downstream of the Estrogen Receptor Signaling Pathway: Discovery of a Potent and Efficient SRC-3 PROTAC Degrader for Overcoming Endocrine Resistance Breast Cancer. J Med Chem. 2025 Jun 12; 68(11):11516-11542.

Typically exists as solids at room temperature

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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