Art. -Nr.: HY-106159

SB-T-101141

SB-T-101141 is a novel taxane. SB-T-101141 effectively induces a noncanonical ferroptosis to overcome Paclitaxel (HY-B0015) resistance of breast cancer. SB-T-101141 facilitates the production of iron and ferrous ions and ROS. SB-T-101141 stably binds to KHSRP to inhibit the iron-dependent expression of CISD1 related to iron homeostasis. SB-T-101141 synergistically enhances the iron-dependent activation of JNK and PERK pathways via KHSRP. SB-T-101141 suppresses breast tumor growth in MCF-7(PR)/MDA-MB-231(PR) or KHSRP knock-down MCF-7 xenograft mice model.

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CAS. Nr.: 186348-05-0
Formel: C₄₄H₅₅NO₁₇
Molecular Weight:869.90

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (290 KB)

SB-T-101141 Chemical Structure

CAS. Nr.: 186348-05-0

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

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Cellular Effect

Cell Line	Type	Value	Description	References
MCF7	IC₅₀	66.66 nM Compound: 31; SB-T-101141	Cytotoxicity against human paclitaxel-resistant MCF7 cells after 72 hrs by MTT assay Cytotoxicity against human paclitaxel-resistant MCF7 cells after 72 hrs by MTT assay	[PMID: 29468872]

In Vitro

SB-T-101141 (1-3 μM, 12 h) efficiently induces microtubule polymerization and tubulin protein expression in MCF-7 and MDA-MB-453 cells^[1].
SB-T-101141 (1-3 μM, 72 h) has potent cytotoxicity with IC₅₀ of 0.03, 0.8 and 6.5 μM for MCF-7, MDA-MB-453 and MDA-MB-231 cells, respectively, while similar effect on normal MCF-10A cells^[1].
SB-T-101141 (0.001-8 μM, 1-14 days) strongly inhibits cell proliferation and colony formation, and increased cell death in MCF-7 and MDA-MB-453 cells^[1].
SB-T-101141 (9 μM, 5 days) effectively inhibits the growth of patient breast cancer organoids^[1].
SB-T-101141 (1-8 μM, 12-60 h) significantly induces cell apoptosis and G2/M phase arrest at 1 μM (no efficacy at high dose), without level changes of cleavages of PARP and caspase-7 in MCF-7 and MDA-MB-453 cells^[1].
SB-T-101141 (3-16 μM, 4-72 h) induces a ferroptosis-like cell death morphology with a low accumulation and increase of membrane permeability, and this effect is markedly blocked by Z-VAD-FMK and Necrostatin-1, with a mild effect on mitochondria numbers and ATP level in MCF-7 and MDA-MB-453 cells^[1].
SB-T-101141 (0.17-8 μM, 0-48 h) significantly increases intracellular iron and ferrous ion as well as MDA level, and reduces GSH level without obvious effect on GPX4 expression in MCF-7, MDA-MB-453 and MCF-7PR cells^[1].
SB-T-101141 (0.17-16 μM, 3-48 h) induces the total ROS (neutralized by DFOM and NAC), lipid ROS, membrane permeability the impaired cell viability and cell death, not be attenuated by DFOM, Fer-1, or Lip-1, in MCF-7, MDA-MB-453, MCF-7PR and MDA-MB-453PR cells^[1].
SB-T-101141 (3-5 nM, 14 days) significantly inhibits Paclitaxel-resistant MCF-7PR and MDA-MB-231PR cells proliferation^[1].
SB-T-101141 (0.25-1.5 μM, 24 h) induces Paclitaxel-resistant cell death and this effect is only only efficiently inhibited by iron chelators DFOM and CPX in MCF-7PR and MDA-MB-453PR cells^[1].
SB-T-101141(0.001-3 μM, 1-14 days) is more sensitive to MCF-7 cellular with knocking down KHSRP than knocking down HDGF and CYP2S1^[1].
SB-T-101141 (0.01-100 μM, 2-24 h) enhances the thermal stability of KHSRP protein without influence on KHSRP expression in MCF-7 cells^[1].
SB-T-101141 (1.5-3 μM, 0-24 h) promotes lipid peroxidation and effectively reduced the mRNA and protein level of CISD1while increase of 4-HNE level via KHSRP in MCF-7 and MCF-7PR cells^[1].
SB-T-101141 (10 μM, 4 h) prominently exertes ER stress-related G3BP1 granule aggregation, without affecting G3BP1 expression^[1].
SB-T-101141 (0.17-16 μM, 24-48 h) increases protein level of eIF2α and induces cell death via the iron-dependent JNK and PERK signaling with in MCF-7, MDA-MB-453, MCF-7PR and MDA-MB-231PR cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[1]

Cell Line:

MCF-7 cells, MDA-MB-453 cells
Concentration:

3  μM (MCF-7 cells), 8  μM (MDA-MB-453 cells)
Incubation Time:

12, 24, 36, 48, 60, 72 h
Result:

Efficiently increased cell death in MCF-7 and MDA-MB-453 cells.
Induced cell death but this effect was reversed by apoptosis inhibitor (Z-VAD-FMK) (HY-16658B) and necrosis inhibitor (Necrostatin-1) (HY-15760).
Significantly increased Paclitaxel-resistant MCF-7PR and MDA-MB-231PR cells survival with IC₅₀ of 2.7 and 0.235 μM, respectively.

Immunofluorescence^[1]

Cell Line:

MCF-7 cells, MDA-MB-453 cells
Concentration:

1 μM
Incubation Time:

12 h
Result:

Efficiently induced microtubule polymerization.

Western Blot Analysis^[1]

Cell Line:

MCF-7 cells, MDA-MB-453 cells
Concentration:

1,3 5 μM (MCF-7 cells), 8 μM (MDA-MB-453 cells)
Incubation Time:

12, 24, 36, 48, 60 h
Result:

Significantly increased the tubulin protein expression in MCF-7 cells at 12 h.
Induced no cleavages of PARP and caspase-7 protein expression changes during 12-60 h in MCF-7 and MDA-MB-453 cells.

Cell Proliferation Assay^[1]

Cell Line:

MCF-7 cells, MDA-MB-453 cells
Concentration:

1 nM, 2  μM (MCF-7 cells), 1 nM, 5  μM (MDA-MB-453 cells)
Incubation Time:

1, 14 days
Result:

Significantly decreased cell proliferation at 1 day in MCF-7 and MDA-MB-453 cells.
Strongly inhibited colony formation at 1 nM after 14 days in MCF-7 and MDA-MB-453 cells.

Apoptosis Analysis^[1]

Cell Line:

MCF-7 cells, MDA-MB-453 cells
Concentration:

1 μM
Incubation Time:

48 h
Result:

Significantly induced cell apoptosis with late apoptosis population from 7.38% to 17.81% in MCF-7 cells and MDA-MB-453 cells (10.51% to 30.76%).

Cell Cycle Analysis^[1]

Cell Line:

MCF-7 cells, MDA-MB-453 cells
Concentration:

1,3 μM (MCF-7 cells), 1,8 μM (MDA-MB-453 cells)
Incubation Time:

24 h
Result:

Significantly induced G2/M phase arrest with G2/M phase population from 11.67% and 9.26% to 23.02% and 28.37% at 1 μM in MCF-7 and MDA-MB-453 cells, respectively.
Induced no G2/M phase arrest at high dose of 3 and 8 μM in MCF-7 and MDA-MB-453 cells, respectively.

In Vivo

SB-T-101141 (5  mg/kg, i.p., once every three days) strongly represses tumor growth in MCF-7(PR)/ MDA-MB-453(PR) xenografted tumor mice mode, without side effects on body weight.^[1].
SB-T-101141 (5  mg/kg, i.p., once every three days) induces no inhibitory activity in tumor growth without increase of aldehyde 4-HNE level in KHSRP knock-down MCF-7 xenografted mice model^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Female immune-deficient BALB/c nude mice (4 weeks old) were injected subcutaneously with Estradiol cypionate (HY-B1100) following with MCF-7 cells (5 × 10⁶ cells/mouse) or MDA-MB-453 cells (1 × 10⁷ cells/mouse)^[1].
Dosage:

5 mg/kg, Estradiol cypionate (1.5 mg/kg)
Administration:

i.p., once every three days (Estradiol cypionate, once every seven days) and then measured body weight and tumor volume.
Result:

Strongly repressed tumor growth in MCF-7/ MDA-MB-453 xenografted tumor mice model.
Caused no significant mouse body weight changes in MDA-MB-453 xenografted tumor mice model.
Had a strong antitumor effect on the Paclitaxel-resistant cell xenografted tumor progression without side effects on body weight.

Animal Model:

Female immune-deficient BALB/c nude mice (4 weeks old) were injected subcutaneously with Estradiol cypionate following with KHSRP knock-down MCF-7 cells (6 × 10⁶ cells/mouse)^[1].
Dosage:

5 mg/kg, Estradiol cypionate (1.5 mg/kg)
Administration:

i.p., once every three days (Estradiol cypionate, once every seven days) and then measured body weight and tumor volume.
Result:

Induced no inhibitory activity in tumor growth without increase of lipid peroxidation product, aldehyde 4-HNE in KHSRP knock-down MCF-7 xenografted mice model

Chemical Information

CAS. Nr. 186348-05-0
Molecular Weight 869.90
Formel C₄₄H₅₅NO₁₇
SMILES

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
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (290 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Zhang X,et al. 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. [Content Brief]

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

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1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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SB-T-101141

Alle p38 MAPK Isoform-spezifische Produkte anzeigen

Alle JNK Isoform-spezifische Produkte anzeigen