SB-T-101141 (1-3 μM, 12 hours) effectively induced microtubule polymerization and tubulin expression in MCF-7 and MDA-MB-453 cells [1]. SB-T-101141 (1-3 μM, 72 hours) showed significant cytotoxicity against MCF-7, MDA-MB-453 and MDA-MB-231 cells, with IC50 values of 0.03, 0.8 and 6.5 μM, respectively, and also had similar effects on normal MCF-10A cells [1]. SB-T-101141 (0.001-8 μM, 1-14 days) strongly inhibited the proliferation and colony formation of MCF-7 and MDA-MB-453 cells and increased cell death [1]. SB-T-101141 (9 μM, 5 days) effectively inhibited the growth of organoids from breast cancer patients [1]. SB-T-101141 (1-8 μM, 12-60 h) at a concentration of 1 μM can significantly induce apoptosis and G2/M phase arrest in MCF-7 and MDA-MB-453 cells (high doses are ineffective) without affecting the cleavage levels of PARP and caspase-7 [1]. SB-T-101141 (3-16 μM, 4-72 h) can induce a cell death morphology similar to ferroptosis, accompanied by a small amount of cell membrane accumulation and increased membrane permeability. This effect can be significantly blocked by Z-VAD-FMK and Necrostatin-1, and has little effect on the number of mitochondria and ATP levels in MCF-7 and MDA-MB-453 cells [1]. SB-T-101141 (0.17-8 μM, 0-48 h) significantly increased intracellular iron, ferrous ions and MDA levels in MCF-7, MDA-MB-453 and MCF-7PR cells and decreased GSH levels, but had no significant effect on GPX4 expression [1]. SB-T-101141 (0.17-16 μM, 3-48 h) induced an increase in total ROS (which can be neutralized by DFOM and NAC), lipid ROS and membrane permeability in MCF-7, MDA-MB-453, MCF-7PR and MDA-MB-453PR cells, impaired cell viability and caused cell death, and these effects could not be attenuated by DFOM, Fer-1 or Lip-1 [1]. SB-T-101141 (3-5 nM, 14 days) significantly inhibited the proliferation of paclitaxel-resistant MCF-7PR and MDA-MB-231PR cells [1]. SB-T-101141 (0.25-1.5 μM, 24 h) induced death in paclitaxel-resistant cells, and this effect was only effectively inhibited by the iron chelators DFOM and CPX (MCF-7PR and MDA-MB-453PR cells) [1]. Compared with MCF-7 cells with knockdown of HDGF and CYP2S1, MCF-7 cells with knockdown of KHSRP were more sensitive to SB-T-101141 (0.001-3 μM, 1-14 days) [1]. SB-T-101141 (0.01-100 μM, 2-24 h) enhanced the thermostability of KHSRP protein in MCF-7 cells without affecting KHSRP expression [1]. SB-T-101141 (1.5-3 μM, 0-24 h) can promote lipid peroxidation through KHSRP, effectively reduce the mRNA and protein levels of CISD1 in MCF-7 and MCF-7PR cells, and increase the level of 4-HNE [1]. SB-T-101141 (10 μM, 4 h) can significantly promote the aggregation of endoplasmic reticulum stress-related G3BP1 particles without affecting the expression of G3BP1 [1]. SB-T-101141 (0.17-16 μM, 24-48 h) can increase the level of eIF2α protein and induce cell death in MCF-7, MDA-MB-453, MCF-7PR and MDA-MB-231PR cells through iron-dependent JNK and PERK signaling pathways [1].

SB-T-101141 (5 mg/kg, intraperitoneal injection, every three days) significantly inhibited tumor growth in a mouse model of MCF-7(PR)/MDA-MB-453(PR) xenografts without affecting body weight. [1] In a KHSRP-knockdown mouse model of MCF-7 xenografts, SB-T-101141 (5 mg/kg, intraperitoneal injection, every three days) did not inhibit tumor growth and did not increase the level of aldehyde 4-HNE. [1]

Cell viability assay [1]
Cell Types: MCF-7 cells, MDA-MB-453 cells
Tested Concentrations: 3 μM (MCF-7 cells), 8 μM (MDA-MB-453 cells)
Incubation Duration: 12, 24, 36, 48, 60, 72 hours
Experimental Results: Effectively increased the death of MCF-7 and MDA-MB-453 cells. Induced cell death, but this effect could be reversed by the apoptosis inhibitor (Z-VAD-FMK) ( ) and the necrosis inhibitor (Necrostatin-1) ( ). Significantly improved the survival rate of paclitaxel-resistant MCF-7PR and MDA-MB-231PR cells, with IC50 values of 2.7 and 0.235 μM, respectively.

---

Immunofluorescence [1]
Cell Types: MCF-7 cells, MDA-MB-453 cells
Tested Concentrations: 1 μM
Incubation Duration: 12 hours Experimental
Experimental Results: Effectively induced microtubule polymerization.

---

Western Blot Analysis [1]
Cell Types: MCF-7 cells, MDA-MB-453 cells
Tested Concentrations: 1, 3, 5 μM (MCF-7 cells), 8 μM (MDA-MB-453 cells)
Incubation Duration: 12, 24, 36, 48, 60 hours
Experimental Results: After 12 hours, tubulin expression in MCF-7 cells increased significantly. The expression of PARP and caspase-7 proteins remained unchanged in both MCF-7 and MDA-MB-453 cells between 12 and 60 hours.

Animal/Disease Models:Four-week-old female immunodeficient BALB/c nude mice were subcutaneously injected with estradiol cyclopentylpropionate, followed by injection of MCF-7 cells (5 × 10⁶ cells/mouse) or MDA-MB-453 cells (1 × 10⁷ cells/mouse) [1].
Doses: 5 mg/kg, estradiol cyclopentylpropionate (1.5 mg/kg)
Route of Administration: Intraperitoneal injection every three days (estradiol cyclopentylpropionate every seven days), followed by measurement of body weight and tumor volume.
Experimental Results: Tumor growth was significantly inhibited in the MCF-7/MDA-MB-453 xenograft mouse model. No significant change in body weight was observed in the MDA-MB-453 xenograft mouse model. It has a strong anti-tumor effect on the progression of paclitaxel-resistant xenograft tumors and has no side effects on weight.

---

Animal/Disease Models:Four-week-old female immunodeficient BALB/c nude mice were subcutaneously injected with estradiol cyclopentylpropionate, followed by transplantation of KHSRP-knockdown MCF-7 cells (6 × 10⁶ cells/mouse) [1].
Doses: 5 mg/kg, estradiol cyclopentylpropionate (1.5 mg/kg).
Route of Administration: Intraperitoneal injection every three days (estradiol cyclopentylpropionate every seven days), followed by measurement of body weight and tumor volume.
Experimental Results: No inhibitory effect on tumor growth was observed in the KHSRP-knockdown MCF-7 xenograft mouse model, nor was an increase in the lipid peroxidation product aldehyde 4-HNE observed.

[1]. A novel taxane SB-T-101141 triggers a noncanonical ferroptosis to overcome Paclitaxel resistance of breast cancer via iron homeostasis-related KHSRP. Cell Death Dis. 2025 May 19; 16(1):403.

C44H55NO17

869.90

186348-05-0

Typically exists as solids at room temperature

CC1(C)[C@@]2(O3)[C@@H](OC3=O)[C@H](OC([C@H](O)[C@@H](NC(OC(C)(C)C)=O)/C=C(C)/C)=O)C(C)=C1[C@@H](OC(C)=O)C([C@@]4(C)[C@]([C@@](CO5)(OC(C)=O)[C@H]5C[C@@H]4O)([H])[C@@H]2OC(C6=CC=CC=C6)=O)=O

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.

---

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).

View More

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)

---

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).

View More

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

---

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.

---

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