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.

For research use only. We do not sell to patients.

CAS No.: 931305-29-2
Formula: C₂₁H₂₁N₃O₃S
Molecular Weight:395.48

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

Bt354 Chemical Structure

CAS No.: 931305-29-2

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Biological Activity
- Description
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
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Biological Activity

Description

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
Molecular Weight 395.48
Formula C₂₁H₂₁N₃O₃S
SMILES

O=C(NCC=1C=NC=CC1)C2=CC=C(C(=C2)NS(=O)(=O)C3=CC=C(C=C3)C)C
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Room temperature in continental US; may vary elsewhere.
Storage

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

Purity & Documentation

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]

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