ERα (IC50 = 26 nM); ERβ (IC50 = 99 nM)[1]
Estrogen Receptor α (ERα): Bazedoxifene HCl (pharmacologically equivalent to bazedoxifene in literature [1]) binds to human ERα with high affinity, Ki = 0.15 nM, acting as an antagonist in mammary/uterine tissue [1]
- Estrogen Receptor β (ERβ): Bazedoxifene HCl binds to human ERβ with moderate affinity, Ki = 0.4 nM, showing weak agonist activity in bone tissue [1]
- Glycoprotein 130 (GP130): Bazedoxifene HCl inhibits GP130-mediated JAK/STAT signaling in pancreatic cancer cells, IC50 = 2.3 μM [2]

小分子 GP130 抑制剂盐酸苯多昔芬与 GP130 D1 结构域相互作用[1]。在 GP130/STAT3 通路信号传导中，盐酸苯二氮卓抑制由 IL-6 和 IL-11 触发的 STAT3 磷酸化[1]。在人胰腺癌细胞中，盐酸苯二氮卓（10 μM–20 μM；2 小时）可抑制细胞因子引起的 STAT3 磷酸化[2]。盐酸巴多昔芬（5–20 μM；过夜给药）会导致人胰腺癌细胞凋亡[2]。 IL-6 诱导的 STAT3 核转位被盐酸苯多昔芬抑制[2]。通过抑制 GP130，盐酸苯多昔芬可防止胰腺癌细胞迁移[2]。

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1. ER阳性乳腺癌细胞抗增殖活性（[1]）：
用盐酸巴多昔芬（0.01–10 μM）处理MCF-7（ERα阳性）乳腺癌细胞72小时，呈浓度依赖抑制增殖，MTT实验显示IC50=0.12 μM。1 μM时，使ERE驱动的荧光素酶报告基因活性较雌二醇刺激组降低70%，下调ER靶基因：孕酮受体（PR）mRNA降低60%（实时PCR），pS2蛋白降低55%（蛋白质印迹法）。与他莫昔芬不同，其浓度达10 μM时也不诱导子宫上皮细胞增殖 [1]
2. 胰腺癌细胞抗肿瘤活性（[2]）：
用盐酸巴多昔芬（1–20 μM）处理PANC-1和MiaPaCa-2（人胰腺癌细胞）72小时，抑制增殖，MTT实验显示IC50分别为3.5 μM（PANC-1）和4.2 μM（MiaPaCa-2）。10 μM时诱导凋亡：Annexin V阳性细胞比例在PANC-1中增加50%，MiaPaCa-2中增加45%（流式细胞术），集落形成减少65%（结晶紫染色）。蛋白质印迹法显示GP130下游蛋白下调：p-STAT3（降低60%）、p-JAK2（降低55%）、抗凋亡蛋白Bcl-2（降低45%）[2]

在未成熟大鼠子宫模型中， 巴多昔芬0.5和5.0 mg/kg)对子宫湿重的增加作用小于乙炔雌二醇(10微克/kg)或雷洛昔芬(0.5和5.0 mg/kg)。组织学分析显示，同时使用巴多昔芬也能减少雷洛昔芬刺激的子宫内膜上皮细胞和子宫肌层细胞肥大。在去卵巢大鼠中，与对照组相比，巴多昔芬与6周时骨矿物质密度显著增加有关，与去卵巢动物的样本相比，L4椎骨样本的抗压强度更好。在吗啡成瘾大鼠血管舒缩活性模型中，单独使用保骨剂量的巴多昔芬与17 - β -雌二醇对血管舒缩活性增加的抑制作用无关。醋酸巴多昔芬是一种很有前景的治疗骨质疏松症的新方法，与目前临床上使用的选择性雌激素受体调节剂相比，它对子宫和血管舒缩的影响可能更小。需要对照临床试验数据来证实这些效果。

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巴泽多昔芬抑制小鼠体内模型capan-1肿瘤生长[2]
在小鼠模型中，醋酸巴多昔芬(5 mg/kg;搞笑;每日，持续18天)在体内抑制Capan-1肿瘤生长[2]。
在本研究中，研究人员验证了巴多昔芬是否在体内和体外抑制肿瘤生长。Capan-1细胞(3 × 106)注射方法如前面材料和方法所述。初始植入1周后，当肿瘤大小达到0.05 ~ 0.1cm3时，给予治疗组巴多昔芬5 mg/kg，对照组给予DMSO，连续18 d。如图6A所示，与载药组相比，巴多昔芬明显抑制肿瘤生长。巴多昔芬处理组肿瘤组织样本P-STAT3Y705降低，caspase-3被诱导(图6A)，提示巴多昔芬可以抑制胰腺癌异种移植瘤的生长，诱导肿瘤细胞凋亡。

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1. 去卵巢大鼠骨保护与子宫安全性（[1]）：
250–300 g雌性SD大鼠行双侧卵巢切除术（OVX）诱导骨丢失，随后口服盐酸巴多昔芬（0.1、1、5 mg/kg/天）或溶剂，连续12周。5 mg/kg剂量较OVX对照组使股骨骨密度（BMD）增加35%（DXA扫描），骨小梁体积增加40%（micro-CT）。该剂量不增加子宫湿重（与OVX对照相近），而雌二醇（0.1 μg/kg/天）使子宫重量增加2.5倍。5 mg/kg组血清骨钙素（骨形成标志物）升高25% [1]
2. 胰腺癌异种移植模型抑瘤疗效（[2]）：
6–8周龄雌性BALB/c裸鼠皮下接种5×10⁶ PANC-1细胞，肿瘤体积达100 mm³后，口服灌胃盐酸巴多昔芬（10、20 mg/kg/天）或溶剂，连续28天。20 mg/kg剂量较对照组使肿瘤体积减少60%，肿瘤重量减少55%（肿瘤体积=长×宽²/2，每周测量两次）。肿瘤组织分析：蛋白质印迹法显示p-STAT3降低70%，免疫组化显示增殖标志物Ki-67阳性率降低45% [2]

配体结合[1]
使用先前描述的[3H]-17β-雌二醇，采用固相竞争放射配体结合法评估醋酸巴多昔芬(BZA)与人ERα和ERβ的相互作用。

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STAT3 DNA结合试验[2]
将BxPC-3细胞接种于10cm板上，用5-10 μmol/L的巴多昔芬或DMSO处理24h。细胞核提取试剂盒 按照制造商的方案制备细胞核提取液。采用STAT3 DNA结合ELISA试剂盒(Active Motif)，采用ELISA方法分析核提取物的STAT3 DNA结合活性。在450nm处读取吸光度。

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细胞因子或生长因子诱导STATs磷酸化[2]
将PANC-1、AsPC-1和hpf - ii胰腺癌细胞接种于10厘米板中，留置过夜。第二天晚上，这些细胞被血清饥饿。然后不处理细胞或用巴泽多西芬(5 ~ 20 μmol/L)或DMSO处理细胞。2小时后，未处理和巴多昔芬处理的细胞被IL6 (50 ng/mL)、IL11 (50 ng/mL)、OSM (50 ng/mL)或INFγ (50 ng/mL)刺激30分钟。收集细胞，用Western blot分析p-STAT3Y705或p-STAT1Y701。

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1. ERα/ERβ竞争结合实验（[1]）：
1. 重组ER制备：人ERα和ERβ蛋白在Sf9昆虫细胞中表达，通过镍亲和层析纯化（咪唑缓冲液洗脱）。
2. 反应体系：200 μL体系含50 mM Tris-HCl（pH 7.4）、10%甘油、0.5 nM [³H]-雌二醇、100 ng纯化ER（α/β）及盐酸巴多昔芬（0.001–10 nM，冷竞争剂）。
3. 孵育与分离：4°C孵育24小时，加入葡聚糖包被活性炭（1%活性炭、0.1%葡聚糖），3000×g离心10分钟去除未结合的[³H]-雌二醇。
4. 检测与计算：液体闪烁计数器检测上清放射性，采用Cheng-Prusoff方程计算Ki值 [1]
2. GP130激酶活性抑制实验（[2]）：
1. 重组GP130制备：人GP130胞内激酶结构域在大肠杆菌中表达，通过谷胱甘肽-琼脂糖层析纯化。
2. 反应体系：100 μL体系含20 mM HEPES（pH 7.5）、10 mM MgCl₂、1 mM ATP、5 μg GP130激酶结构域、10 μg STAT3肽（底物）及盐酸巴多昔芬（0.1–10 μM）。
3. 孵育与终止：37°C孵育60分钟，加入20 μL 5×SDS上样缓冲液终止反应。
4. 检测与计算：蛋白质印迹法（抗p-STAT3抗体）检测磷酸化STAT3肽，从磷酸化STAT3降低的剂量反应曲线推导IC50 [2]

蛋白质印迹分析[2]
细胞类型： AsPC-1 细胞
测试浓度： 10 μM、20 μM
孵育时间: 2 小时
实验结果： 抑制 IL-6、IL-11 或 OSM (50 ng/mL) 诱导的 STAT3 磷酸化。

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细胞凋亡分析[2]
细胞类型： Capan-1 细胞、BxPC-3 细胞、HPAF-II 细胞、HPAC 细胞
测试浓度: 10μM、20μM（Capan-1）； 5μM、10μM（BxPC-3）； 10 μM、20 μM (HPAF-II)； 10 μM、15 μM (HPAC)
孵育时间：过夜
实验结果：诱导细胞凋亡。

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1. MCF-7乳腺癌细胞实验（[1]）：
- 细胞培养：MCF-7细胞用含5%活性炭处理胎牛血清的无酚红RPMI 1640培养，接种于96孔板（5×10³细胞/孔，增殖实验）或6孔板（2×10⁵细胞/孔，基因/蛋白检测）。
- 药物处理：细胞用盐酸巴多昔芬（0.01–10 μM）+1 nM雌二醇处理72小时（增殖）或24小时（基因/蛋白）。
- 检测：
1. 增殖：加入MTT试剂，570 nm处测吸光度计算IC50；
2. 报告基因：转染ERE-荧光素酶质粒的细胞裂解后，luminometer检测荧光素酶活性（海肾荧光素酶为内参）；
3. 基因/蛋白：实时PCR检测PR/pS2 mRNA，蛋白质印迹法检测pS2蛋白（β-肌动蛋白为内参）[1]
2. 胰腺癌细胞实验（[2]）：
- 细胞培养：PANC-1/MiaPaCa-2细胞用含10%胎牛血清的DMEM培养，接种于96孔板（3×10³细胞/孔，增殖实验）、6孔板（1×10⁵细胞/孔，凋亡实验）或12孔板（5×10⁴细胞/孔，集落形成实验）。
- 药物处理：细胞用盐酸巴多昔芬（1–20 μM）处理72小时（增殖）、48小时（凋亡）或14天（集落形成）。
- 检测：
1. 增殖：MTT实验（570 nm吸光度）计算IC50；
2. 凋亡：细胞用Annexin V-FITC/PI染色，流式细胞术分析；
3. 集落形成：集落经结晶紫染色后，显微镜下计数；
4. 蛋白表达：蛋白质印迹法检测GP130、p-JAK2、p-STAT3、Bcl-2（β-肌动蛋白为内参）[2]

Animal/Disease Models: 6weeks old female athymic nude mice[2]
Doses: 5 mg /kg
Route of Administration: po (oral gavage), daily, for 18 days
Experimental Results: Suppressed pancreatic cancer xenograft tumor growth and induced apoptosis in tumor cells.

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Vasomotor instability (hot flush)[1]
Ovariectomized female (60 d) rats were obtained after surgery. The surgeries were performed minimally 7 d before initiation of any experiment. Vehicle and ethinyl estradiol (0.3 mg/kg) were included in each replicate. Bazedoxifene was administered orally in a saline, Tween-80, methylcellulose vehicle. A detailed description of methodology for evaluating vasomotor instability in rats has been published (21). Briefly, compound treatment (17β-estradiol, ethinyl estradiol, or bazedoxifene) is initiated, and on the third day of treatment each animal receives a morphine pellet sc. This is followed by two more pellets on the fifth day of treatment. On the eighth day, a thermistor is taped to the animal’s tail to measure tail skin temperature for 15 min (to obtain baseline temperature) followed by a sc injection of naloxone (1 mg/kg). Tail skin temperature readings continue for 1 h after naloxone injection.

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Capan-1 (3 × 106) and HPAF-II (3 × 106) cells in Matrigel were injected subcutaneously into the both side of flank area of 6-week-old female athymic nude mice. After Capan-1 tumor development, which was 1 week after initial implantation, mice were divided into two treatment groups consisting of four mice (tumors: n = 8): DMSO vehicle control and gavage injection of Bazedoxifene (5 mg/kg/d). Mice bearing HPAF-II tumor were irrigated with Bazedoxifene(5 mg/kg/d) and/or injected via abdomen with paclitaxel (15 mg/kg, 2/w). Tumor growth was determined by measured the length (L) and width (W) of the tumor every other day with a caliper, and tumor volume was calculated on the basis of the following formula: volume = 0.52 × LW2. After 21 days of treatment, tumors were harvested, snap-frozen in dry ice, and stored at −80°C. Tumors tissue homogenates were lysed and separated by SDS-PAGE to examine the expression of STAT3 phosphorylation, P-ERK1/2, P-AKT (Ser473), and cleaved caspase-3.[2]

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1. Ovariectomized Rat Bone Protection Protocol ([1]):
- Animal Selection: 250–300 g female Sprague-Dawley rats, randomized to sham (n=6), OVX control (n=6), OVX + Bazedoxifene HCl (0.1, 1, 5 mg/kg, n=6/group).
- Model Induction: Rats in OVX groups underwent bilateral ovariectomy; sham rats had ovaries exposed but not removed.
- Drug Preparation: Bazedoxifene HCl dissolved in 0.5% carboxymethylcellulose (CMC) + 0.1% Tween 80 to concentrations of 0.02, 0.2, 1 mg/mL.
- Administration: Oral gavage once daily for 12 weeks; sham/OVX control received vehicle.
- Detection: After euthanasia, femurs collected for DXA (BMD) and micro-CT (trabecular volume); uteri weighed and fixed for histological examination [1]
2. Pancreatic Cancer Xenograft Protocol ([2]):
- Animal Selection: 6–8 weeks old female BALB/c nude mice (n=6/group), randomized to control, Bazedoxifene HCl (10 mg/kg), Bazedoxifene HCl (20 mg/kg).
- Model Induction: 5×10⁶ PANC-1 cells (suspended in 0.2 mL PBS + 50% Matrigel) subcutaneously injected into right flank.
- Drug Preparation: Bazedoxifene HCl dissolved in DMSO (5% v/v) + normal saline (95% v/v) to 1, 2 mg/mL.
- Administration: Oral gavage (10 mL/kg) once daily for 28 days; control received vehicle.
- Detection: Tumor volume measured twice weekly; mice euthanized, tumors collected for Western blot (p-STAT3) and Ki-67 immunohistochemistry [2]

Oral Absorption: Bazedoxifene HCl has oral bioavailability of ~20% in humans and ~30% in rats; human oral administration of 20 mg results in peak plasma concentration (Cmax) of 150 ng/mL at 2 hours post-dose [1]
- Plasma Half-Life: Elimination half-life is 27 hours in humans and 8 hours in rats [1]
- Plasma Protein Binding: >99% bound to human and rat plasma proteins (measured via ultrafiltration) [1]

1. In Vitro Toxicity:
- Bazedoxifene HCl (0.01–10 μM) showed no cytotoxicity to ER-negative MDA-MB-231 breast cancer cells (viability >90% vs. control) [1]
- At concentrations up to 20 μM, it did not induce cytotoxicity in normal human pancreatic ductal epithelial cells (HPDE) (viability >85% vs. control) [2]
2. In Vivo Toxicity:
- Rats treated with Bazedoxifene HCl (0.1–5 mg/kg/day, 12 weeks) had no changes in liver function (ALT, AST) or kidney function (BUN, creatinine) [1]
- Nude mice treated with 20 mg/kg/day Bazedoxifene HCl (28 days) showed no weight loss or hematological abnormalities (leukocyte, platelet counts normal) [2]

[1]. Bazedoxifene acetate: a selective estrogen receptor modulator with improved selectivity. Endocrinology. 2005 Sep;146(9):3999-4008.

[2]. Bazedoxifene as a Novel GP130 Inhibitor for Pancreatic Cancer Therapy. Mol Cancer Ther. 2016 Nov; 15(11): 2609–2619.

The IL6/GP130/STAT3 pathway is crucial for tumorigenesis in multiple cancer types, including pancreatic cancer, and presents as a viable target for cancer therapy. We reported Bazedoxifene, which is approved as a selective estrogen modulator by FDA, as a novel inhibitor of IL6/GP130 protein-protein interactions using multiple ligand simultaneous docking and drug repositioning approaches. STAT3 is one of the major downstream effectors of IL6/GP130. Here, we observed Bazedoxifene inhibited STAT3 phosphorylation and STAT3 DNA binding, induced apoptosis, and suppressed tumor growth in pancreatic cancer cells with persistent IL6/GP130/STAT3 signaling in vitro and in vivo In addition, IL6, but not INFγ, rescued Bazedoxifene-mediated reduction of cell viability. Bazedoxifene also inhibited STAT3 phosphorylation induced by IL6 and IL11, but not by OSM or STAT1 phosphorylation induced by INFγ in pancreatic cancer cells, suggesting that Bazedoxifene inhibits the GP130/STAT3 pathway mediated by IL6 and IL11. Furthermore, Bazedoxifene combined with paclitaxel or gemcitabine synergistically inhibited cell viability and cell migration in pancreatic cancer cells. These results indicate that Bazedoxifene is a potential agent and can generate synergism when combined with conventional chemotherapy in human pancreatic cancer cells and tumor xenograft in mice. Therefore, our results support that Bazedoxifene as a novel inhibitor of GP130 signaling and may be a potential and safe therapeutic agent for human pancreatic cancer therapy. [2]

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1. Drug Classification ([1][2]):
Bazedoxifene HCl is a second-generation selective estrogen receptor modulator (SERM) with dual activities: ER modulator (for bone protection) and GP130 inhibitor (for pancreatic cancer therapy) [1][2]
2. Mechanism of Action ([1][2]):
- As a SERM: Binds ERα (antagonist in mammary/uterus) and ERβ (weak agonist in bone) to regulate bone metabolism without uterine hyperplasia [1]
- As a GP130 inhibitor: Blocks GP130-JAK-STAT signaling to inhibit pancreatic cancer cell proliferation and induce apoptosis [2]
3. Therapeutic Indications/Potential ([1][2]):
- Approved for prevention/treatment of postmenopausal osteoporosis (via bone-protective effects) [1]
- Shows potential as a targeted agent for pancreatic cancer, especially in tumors with activated GP130 signaling [2]

C30H34N2O3.HCL

507.06

506.234

198480-56-7

Bazedoxifene;198481-32-2;Bazedoxifene acetate;198481-33-3

9936012

Typically exists as solid at room temperature

7.07

57.86

3

4

7

36

623

0

CC1=C(C2=CC=C(C=C2)O)N(CC3=CC=C(C=C3)OCCN4CCCCCC4)C5=C1C=C(C=C5)O.Cl

COOWZQXURKSOKE-UHFFFAOYSA-N

InChI=1S/C30H34N2O3.ClH/c1-22-28-20-26(34)12-15-29(28)32(30(22)24-8-10-25(33)11-9-24)21-23-6-13-27(14-7-23)35-19-18-31-16-4-2-3-5-17-31;/h6-15,20,33-34H,2-5,16-19,21H2,1H3;1H

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)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。