Cat. No.: HY-155949

Bt354

Bt354 is an orally active STAT3 inhibitor with IC₅₀ values of 4.6 μM (DU145), 6.5 μM (MDA-MB-435) and 7.2 μM (MDA-MB-231), respectively. Bt354 induces cell cycle arrest and apoptosis, and downregulates epithelial-mesenchymal transition-related genes. Bt354 exhibits anti-angiogenic and anti-inflammatory activities, attenuates the polarization of M1 microglia and A1 astrocytes, suppresses inflammasome-related signaling pathways, and alleviates mechanical hyperalgesia and thermal hyperalgesia. Bt354 can be used in research related to glioblastoma multiforme, triple-negative breast cancer, prostate cancer and neuropathic pain.

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CAS No.: 931305-29-2
화학식: C₂₁H₂₁N₃O₃S
분자량:395.48

보관:

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

Bt354 Chemical Structure

CAS No.: 931305-29-2

Amount: USD 0.00

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Use of MCE Products

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

Biological Activity
- 제품 설명
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

Cellular Effect

Cell Line	Type	Value	Description	References
DU-145	IC₅₀	0.12 μM Compound: 2	Antiproliferative activity against human DU-145 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay Antiproliferative activity against human DU-145 cells assessed as inhibition of cell growth incubated for 72 hrs by MTT assay	[PMID: 36511661]

In Vitro

Bt354 (0.1-100 μM; 24-72 h) exhibits concentration- and time-dependent antiproliferative activity against U87 MG, GBM8401 and T98G glioblastoma cells, with IC₅₀ values of 9.96 μM, 15.18 μM and 3.39 μM, respectively, after 24 h of incubation^[1].
Bt354 (0.01-5 μM; 48 h) induces apoptosis in U87 MG glioblastoma cells in a concentration-dependent manner, and a significant increase in the proportion of apoptotic cells is observed at concentrations of 0.1 μM and above after 48 h of incubation^[1].
Bt354 (0.1-5 μM; 24 h) induces apoptosis in U87 MG glioblastoma cells by upregulating the expression of cleaved caspase-3 and cleaved PARP, and reducing the activity of pro-caspase-3; a significant effect is observed at concentrations of 0.1 μM and above after 24 h of incubation^[1].
Bt354 (0.1-5 μM; 24 h) inhibits epithelial-mesenchymal transition in U87 MG glioblastoma cells by upregulating E-cadherin expression and downregulating the expressions of vimentin, matrix metalloproteinase-2 (MMP-2), ZEB1 and FOXM1; after 24 h of incubation, significant effects are observed at concentrations of 0.1 μM and above (the effective concentrations for E-cadherin and ZEB1 are 1 μM and above)^[1].
Bt354 (0.01-5 μM; 6-18 h) inhibits the migration of U87 MG glioblastoma cells in a concentration- and time-dependent manner. A significant migration-inhibiting effect is observed at concentrations of 0.01 μM and above, and the inhibitory effect reaches the maximum level after 18 h of incubation^[1].
Bt354 (0.1-5 μM; 24 h) alters the polymerization state of F-actin in U87 MG glioblastoma cells, converting filamentous F-actin into a globular form near the nucleus; it inhibits cell migration after 24 h of incubation at concentrations of 0.1 μM and above^[1].
Bt354 (0.1-5 μM; 24 h) regulates epithelial-mesenchymal transition in U87 MG glioblastoma cells by upregulating E-cadherin expression and downregulating vimentin expression, and this effect occurs at concentrations of 0.1 μM or higher after 24 h of incubation^[1].
Bt354 (0.1-5 μM; 24 h) reduces the production of MMP-2 in U87 MG glioblastoma cells in a concentration-dependent manner in vitro, and a significant reduction is observed at concentrations of 0.1 μM and above after 24 h of incubation^[1].
Bt354 (24 h) potently inhibits STAT3-dependent luciferase activity in DU145, MDA-MB-435 and MDA-MB-231 cells, with IC₅₀ values of 4.6 μM, 6.5 μM and 7.2 μM, respectively^[3].
Bt354 (24-72 h) inhibits the proliferation of DU145, MDA-MB-435 and MDA-MB-231 cells in a time- and dose-dependent manner, with its IC₅₀ values ranging from 0.07 μM to 35 μM depending on the cell line and incubation time^[3].
Bt354 specifically inhibits the phosphorylation of STAT3 at the Tyr705 site (without affecting phosphorylation at the Ser727 site or the upstream JAK2/Src signaling pathway), and downregulates the expression of STAT3-dependent pro-proliferative and anti-apoptotic proteins in MDA-MB-435 and MDA-MB-231 cells^[3].
Bt354 (0.1-5 μM; 12 h) inhibits the nuclear translocation of STAT3 in MDA-MB-435 and MDA-MB-231 cells in a dose-dependent manner, which is evidenced by the reduced nuclear STAT3 levels after treatment with 1 μM or 5 μM Bt354 for 12 h^[3].
Bt354 (0.5 μM; 24 h) induces G2/M cell cycle arrest in MDA-MB-435 and MDA-MB-231 cells^[3].
Bt354 (48 h) induces late-stage apoptosis in MDA-MB-435 and MDA-MB-231 cells in a dose-dependent manner, increasing the proportion of late-stage apoptotic cells to 26.0% and 29.5%, respectively^[3].
Bt354 (1 μM) inhibits the migration of MDA-MB-435 and MDA-MB-231 cells in a dose-dependent manner, with a significant inhibitory effect observed at the concentration of 1 μM in MDA-MB-435 cells^[3].

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

Apoptosis Analysis^[1]

Cell Line:

U87 MG glioblastoma cells
Concentration:

0.01, 0.1, 1 and 5 μM
Incubation Time:

24 h; 48 h
Result:

Induced a significant, concentration-dependent increase in the proportion of apoptotic U87 MG cells at concentrations of 0.1 μM to 5 μM after 48 h treatment.
Showed no discernible apoptotic effect after 24 h of treatment at equivalent concentrations.

Western Blot Analysis^[1]

Cell Line:

U87 MG glioblastoma cells
Concentration:

0.1, 1 and 5 μM
Incubation Time:

24 h
Result:

Increased cleaved caspase-3 and cleaved PARP expression levels substantially at 1 μM.
Decreased pro-caspase-3 activity significantly in U87 MG cells treated with 0.1 μM and above.\nIncreased E-cadherin expression in a concentration-dependent manner, with significant increase observed at 1 μM and above.
Decreased vimentin, MMP-2, and FOXM1 expression in a concentration-dependent manner, with significant decreases observed at 0.1 μM and above.
Decreased ZEB1 expression in a concentration-dependent manner, with significant decrease observed at 1 μM and above.
Caused no significant changes in SLUG expression.

Cell Migration Assay ^[1]

Cell Line:

U87 MG glioblastoma cells
Concentration:

0.01, 0.1, 1 and 5 μM
Incubation Time:

6 h; 12 h; 18 h
Result:

Significantly inhibited U87 MG cell migration in a concentration- and time-dependent manner, with significant inhibition observed at 0.01 μM and above.
Increased inhibition over time, with the maximal effect observed at 18 h.

Immunofluorescence^[1]

Cell Line:

U87 MG glioblastoma cells
Concentration:

0.1, 1 and 5 μM
Incubation Time:

24 h
Result:

Altered F-actin polymerization in U87 MG glioblastoma cells, converting filamentous F-actin to a globular form near the nucleus.
Inhibited cell metastasis in treated cells.\nIncreased E-cadherin expression significantly as Bt354 concentration increased.
Decreased vimentin expression significantly with increasing Bt354 concentration.

ELISA Assay^[1]

Cell Line:

U87 MG glioblastoma cells
Concentration:

0.1, 1 and 5 μM
Incubation Time:

24 h
Result:

Reduced MMP-2 concentration in U87 MG cell supernatant in a concentration-dependent manner.
Showed significant effects at 0.1 μM and above.

Immunofluorescence^[3]

Cell Line:

MDA-MB-435 human triple negative breast cancer cells, MDA-MB-231 human triple negative breast cancer cells
Concentration:

0.1, 1 and 5 μM
Incubation Time:

12 h
Result:

Reduced nuclear STAT3 levels substantially in a dose-dependent manner, with STAT3 remaining primarily in the cytoplasm after treatment with 1 μM or 5 μM Bt354 for 12 h.

Cell Cycle Analysis^[3]

Cell Line:

MDA-MB-435 human triple negative breast cancer cells, MDA-MB-231 human triple negative breast cancer cells
Concentration:

0.5 μM
Incubation Time:

24 h
Result:

Caused G2/M phase accumulation, with G2/M percentages increasing to 28.68% (MDA-MB-435) and 27.50% (MDA-MB-231).

In Vivo

Bt354 (0.1-20 μg; i.t.; single injection; 24 hours) and (0.25-1 μg/h; i.t.; continuous infusion; 7-14 days) produces dose-dependent acute and sustained preventive analgesic effects in CCI-induced neuropathic pain in rats by inhibiting neuronal pSTAT3 signaling, reducing neuroinflammation, glial activation, and angiogenesis, with an ED₅₀ of 1.176 μg^[2].
Bt354 (10-40 mg/kg; p.o.; once every 3 days; 21 days) elicits dose-dependent antitumor activity in MDA-MB-231 xenograft mice^[3].
Bt354 (10-40 mg/kg; p.o.; once every 3 days; 21 days) elicits dose-dependent antitumor activity in MDA-MB-435 xenograft mice^[3].

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

Animal Model:

Wistar (adult male, 250-285 g, chronic constriction injury of right sciatic nerve, intrathecal catheter implantation prior to CCI induction)^[2]
Dosage:

0.1-20 μg (acute testing); 0.25-1 μg/h (preventive testing)
Administration:

i.t.; single injection (acute testing); continuous infusion, 7-14 days (preventive testing)
Result:

Produced dose-dependent analgesic effect on CCI-induced thermal hyperalgesia with pharmacodynamic activity lasting up to 24 hours.
Calculated ED₅₀ of 1.176 μg.
Resulted in significantly higher paw withdrawal threshold values than CCI + vehicle controls from day 3 to day 14 post-surgery.
Elevated paw withdrawal latency values relative to CCI + vehicle controls from day 1 to day 14 post-surgery, with dose-dependent improvement observed.
Significantly attenuated CCI-induced upregulation of STAT3 and phosphorylated STAT3 in the ipsilateral spinal cord dorsal horn, including reduced nuclear translocation of neuronal pSTAT3.
Mitigated CCI-induced activation and pro-inflammatory polarization of microglia and astrocytes.
Suppressed neuronal NLRP3 inflammasome expression.
Reduced neuronal LDHA and pTBK1 expression.
Attenuated microglial pCREB and pP38 expression.
Decreased pro-inflammatory cytokine production in neurons and microglia.
Inhibited CCI-induced angiogenesis.

Animal Model:

BalB/c-nu/nu (female, 8-10 week old)^[3]
Dosage:

10 mg/kg; 20 mg/kg; 40 mg/kg
Administration:

p.o.; once every 3 days; 21 days
Result:

Reduced mean tumor volume to 1303.2 mm³ (10 mg/kg), 976.0 mm³ (20 mg/kg), and 811.0 mm³ (40 mg/kg), compared to 2604.3 mm³ in controls.
Achieved tumor growth inhibition (T/C) values of 50%, 37.4%, and 31.3% for the 10, 20, and 40 mg/kg groups, respectively.
Decreased tumor weight by 74.6% in the 40 mg/kg group.
Reduced p-STAT3(Y705) levels in tumor tissue in a dose-dependent manner.
Lowered Ki-67-positive cell counts in all Bt354-treated groups.
Increased tumor cell apoptosis (measured via TUNEL assay) in a dose-dependent manner across all Bt354 groups.\nReduced mean tumor volume to 393.2 mm³ (10 mg/kg), 351.1 mm³ (20 mg/kg), and 321.4 mm³ (40 mg/kg), compared to 1365.8 mm³ in controls.
Achieved tumor growth inhibition (T/C) values of 28.7%, 25.7%, and 23.5% for the 10, 20, and 40 mg/kg groups, respectively.
Decreased tumor weight by 56.2%, 63.8%, and 77.1% in the 10, 20, and 40 mg/kg groups, respectively.
Reduced p-STAT3(Y705) levels in tumor tissue in a dose-dependent manner.
Lowered Ki-67-positive cell counts in all Bt354-treated groups.
Increased tumor cell apoptosis (measured via TUNEL assay) in a dose-dependent manner across all Bt354 groups.

Chemical Information

CAS No. 931305-29-2
분자량 395.48
화학식 C₂₁H₂₁N₃O₃S
SMILES

O=C(NCC=1C=NC=CC1)C2=CC=C(C(=C2)NS(=O)(=O)C3=CC=C(C=C3)C)C
선적

Room temperature in continental US; may vary elsewhere.
보관

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

순도&문서

Handling Instructions (2659 KB)

References

[1]. Chiang YC, et al. STAT3 phosphorylation inhibitor Bt354 exhibits anti-neoplastic activity in glioblastoma multiforme cells. Environ Toxicol. 2024;39(6):3292-3303. [Content Brief]

[2]. Cheng HJ, et al. Intrathecal STAT3 inhibitor Bt354 ameliorates chronic constriction injury-induced nociceptive sensitization by modulating neuroinflammation. Neurotherapeutics. 2025;22(6):e00763. [Content Brief]

[3]. Chen Y, et al. Bt354 as a new STAT3 signaling pathway inhibitor against triple negative breast cancer. J Drug Target. 2018;26(10):920-930. [Content Brief]

Calculators

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

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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