2. 疾病领域
  3. 癌症 神经系统疾病 泌尿生殖系统疾病
  4. 神经系统肿瘤 胶质瘤 乳腺癌 前列腺癌 泌尿生殖系统癌症 疼痛
  5. 胶质母细胞瘤
  6. Bt354

Bt354 是一种具有口服活性的 STAT3 抑制剂，其 IC50 值分别为 4.6 μM (DU145)、6.5 μM (MDA-MB-435) 和 7.2 μM (MDA-MB-231)。Bt354 可诱导细胞周期阻滞和细胞凋亡 (apoptosis)，下调上皮间质转化相关基因。Bt354 具有抗血管生成和抗炎活性，可减弱 M1 小胶质细胞和 A1 星形胶质细胞的极化，抑制炎症小体相关信号通路，并减轻机械性痛觉过敏和热痛觉过敏。Bt354 可用于多形性胶质母细胞瘤、三阴性乳腺癌、前列腺癌和神经病理性疼痛的相关研究。

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Bt354

Bt354 Chemical Structure

CAS No. : 931305-29-2

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Bt354 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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[1][2][3].

体外研究
(In Vitro)

Bt354 (0.1-100 μM; 24-72 h) 对 U87 MG、GBM8401 和 T98G 胶质母细胞瘤细胞表现出浓度和时间依赖性的抗增殖活性，孵育 24 h 后其 IC50 值分别为 9.96 μM、15.18 μM 和 3.39 μM[1]。
Bt354 (0.01-5 μM; 48 h) 以浓度依赖的方式诱导 U87 MG 胶质母细胞瘤细胞发生凋亡，孵育 48 小时后，在 0.1 μM 及以上浓度下可观察到凋亡细胞比例显著升高[1]。
Bt354 (0.1-5 μM; 24 h) 可通过上调活化型半胱天冬酶-3 (cleaved caspase-3) 和活化型多聚腺苷二磷酸核糖聚合酶 (cleaved PARP) 的表达、降低前体半胱天冬酶-3 (pro-caspase-3) 的活性，诱导 U87 MG 胶质母细胞瘤细胞发生凋亡；孵育 24 h 后，0.1 μM 及以上浓度即可观察到显著效应[1]。
Bt354 (0.1-5 μM; 24 h) 可通过上调 E-cadherin 表达、下调波形蛋白 (vimentin)、基质金属蛋白酶-2 (MMP-2)、ZEB1 及 FOXM1 的表达，抑制 U87 MG 胶质母细胞瘤细胞发生上皮间质转化；孵育 24 小时后，0.1 μM 及以上浓度即可观察到显著作用 (E-cadherin 和 ZEB1 对应的有效浓度为 1 μM 及以上)[1]。
Bt354 (0.01-5 μM; 6-18 h) 可呈浓度和时间依赖性抑制 U87 MG 胶质母细胞瘤细胞的迁移，在 0.01 μM 及以上浓度时即可观察到显著的迁移抑制效果，且孵育 18 h 时抑制作用达到最强[1]。
Bt354 (0.1-5 μM; 24 h) 可改变 U87 MG 胶质母细胞瘤细胞中 F-肌动蛋白的聚合状态，将丝状 F-肌动蛋白转化为细胞核附近的球状形式；在 0.1 μM 及以上浓度孵育 24 h 后，该物质可抑制细胞转移[1]。
Bt354 (0.1-5 μM; 24 h) 可通过上调 E-cadherin 表达并下调波形蛋白 (vimentin) 表达，调控 U87 MG 胶质母细胞瘤细胞的上皮-间质转化，该作用在浓度为 0.1 μM 及以上、孵育 24 h 后显现[1]。
Bt354 (0.1-5 μM; 24 h) 可在体外以浓度依赖的方式降低 U87 MG 胶质母细胞瘤细胞中 MMP-2 的产生，孵育 24 h 后在 0.1 μM 及以上浓度下可观察到显著降低[1]。
Bt354 （24 h) 可强效抑制 DU145、MDA-MB-435 和 MDA-MB-231 细胞中 STAT3 依赖的荧光素酶活性，其 IC50 值分别为 4.6 μM、6.5 μM 和 7.2 μM[3]。
Bt354 (24-72 h) 可呈时间和剂量依赖性抑制 DU145、MDA-MB-435 和 MDA-MB-231 细胞的增殖，其 IC50 值根据细胞系和孵育时间的不同在 0.07 μM 至 35 μM 之间变化[3]。
Bt354 可特异性抑制 STAT3 在 Tyr705 位点的磷酸化 (不影响 Ser727 位点的磷酸化或上游 JAK2/Src 信号通路)，并在 MDA-MB-435 和 MDA-MB-231 细胞中下调 STAT3 依赖性促增殖蛋白和抗凋亡蛋白的表达[3]。
Bt354 (0.1-5 μM; 12 h) 可呈剂量依赖性抑制 MDA-MB-435 和 MDA-MB-231 细胞中 STAT3 的核转位，经 1 μM 或 5 μM Bt354 处理 12 h 后细胞核内 STAT3 水平降低的结果可证明这一点[3]。
Bt354 (0.5 μM; 24 h) 可诱导 MDA-MB-435 和 MDA-MB-231 细胞发生 G2/M 期细胞周期阻滞[3]。
Bt354 (48 h) 以剂量依赖方式诱导 MDA-MB-435 和 MDA-MB-231 细胞发生晚期凋亡，分别使晚期凋亡细胞比例升高至 26.0%和 29.5%[3]。
Bt354 (1 μM) 以剂量依赖方式抑制 MDA-MB-435 和 MDA-MB-231 细胞的迁移，在 MDA-MB-435 细胞中 1 μM 浓度下可观察到显著抑制作用[3]。

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

Bt354 相关抗体:

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).
体内研究
(In Vivo)

Bt354 (0.1-20 μg；椎管内注射；单次给药；24 小时；0.25-1 μg/h；椎管内注射；持续输注；7-14 天) 可通过抑制神经元 pSTAT3 信号通路、减轻神经炎症、胶质细胞活化及血管生成，在大鼠 CCI 诱导的神经病理性疼痛模型中产生剂量依赖性的急性和持续性预防性镇痛作用，其 ED50 为 1.176 μg[2]。
Bt354 (10-40 mg/kg；口服；每 3 天 1 次；共 21 天) 在 MDA-MB-231 异种移植小鼠中可诱导剂量依赖性抗肿瘤活性[3]。
Bt354 (10-40 mg/kg；口服；每 3 天 1 次；共 21 天) 在 MDA-MB-435 异种移植小鼠中可诱导剂量依赖性抗肿瘤活性[3]。

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.
分子量

395.48

Formula

C21H21N3O3S
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Bt354 相关分类

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Keywords:

Bt354931305-29-2Bt 354Bt-354U87 MGapoptosisSH2 domainglioblastoma multiformeneuropathic painSTAT3 Y705 phosphorylationepithelial-mesenchymal transitionprostate cancertriple negative breast cancerSTAT3Inhibitorinhibitorinhibit

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