Bexarotene (LGD-1069) is a selective agonist of retinoid X receptors (RXRs), including RXRα, RXRβ, and RXRγ. It exhibits EC50 values of 23 nM for human RXRα, 15 nM for RXRβ, and 27 nM in a RXR-responsive luciferase reporter assay, with no significant activity on retinoic acid receptors (RARs, EC50 > 1000 nM) [1]

Bexarotene 优先结合并激活 RXR 同工型，对于 RXRα、RXRβ 和 RXRγ 同工型，Kd=14±2 nM、21±4 nM 和 29±7 nM [1]。 Bexarotene 可有效减少白血病 (HL-60) 细胞的增殖。 Bexarotene 在 1 μM 时可抑制 HL-60 细胞增殖 37% [1]。 Bexarotene 作为单药处理细胞，在高剂量下显示出抗增殖作用，IC50 为 40.62±0.45 μM (PC3) 和 50.20±4.10 μM (DU145) [2]。 Bexarotene（20 和 40 μM）和多西紫杉醇（5 和 10 μM）在抑制 PC3 和 DU145 细胞生长方面表现出协同作用 [2]。 Bexarotene（20 和 40 μM）抑制 PC3 和 DU145 细胞中细胞周期蛋白 D1 和细胞周期蛋白 D3 的表达 [2]。

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RXR激活实验：在转染RXRα/β/γ表达质粒和RXR响应性荧光素酶报告基因的HEK293细胞中，贝沙罗汀（Bexarotene，LGD-1069）（1-1000 nM）呈剂量依赖性诱导荧光素酶活性。100 nM浓度下，较溶媒对照组，RXRα介导的荧光素酶活性升高8.2倍，RXRβ升高7.5倍，RXRγ升高6.8倍，证实其RXR特异性激动作用[1]
- 前列腺癌细胞抗增殖实验：在人前列腺癌细胞系（PC-3、LNCaP、DU145）中，贝沙罗汀（Bexarotene，LGD-1069）（0.1-10 μM）单药处理72小时（MTT法），IC50分别为1.2 μM（PC-3）、0.8 μM（LNCaP）和1.5 μM（DU145）。与多西他赛（1 nM）联合使用时，协同增强抗增殖效应：联合组PC-3细胞活力降至22%（单药贝沙罗汀组为48%，单药多西他赛组为55%），胱天蛋白酶-3/7活性（凋亡标志物，荧光法检测）升高3.1倍[2]
- 肺癌细胞实验：在小鼠Lewis肺癌（3LL）细胞和人非小细胞肺癌（NSCLC）A549细胞中，贝沙罗汀（Bexarotene，LGD-1069）（0.5-20 μM）抑制集落形成（克隆形成实验）：5 μM浓度下，3LL细胞集落数减少65%，A549细胞集落数减少58%。Western blot显示，5 μM贝沙罗汀处理的3LL细胞中，细胞周期抑制剂p21表达升高2.4倍，细胞周期促进因子Cyclin D1表达降低42%[3]

在帕金森病 (PD) 大鼠模型中，贝沙罗汀（1 mg/kg/天）可有效预防行为缺陷和多巴胺神经元变性的发生，从而显着降低血清 T4 和甘油三酯的变化 [1]。贝沙罗汀是一种能有效阻止肺部肿瘤发展和扩散的药物。在所有三种基因型（p53wt/wtK-raswt/wt、p53val135/wtK-raswt/wt 或 p53wt/wtK-rasko/wt）的小鼠中，贝沙罗汀（灌胃法 100mg/kg）抑制肿瘤多样性和肿瘤体积。贝沙罗汀使 p53wt/wtK-rasko/wt 中腺瘤进展为腺癌的速度降低了约 50%。以及 p53wt/wtK-raswt/wt 的小鼠 [3]。

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前列腺癌异种移植模型：雄性裸鼠（BALB/c nu/nu，6-8周龄）皮下注射5×10⁶个PC-3细胞，待肿瘤达100-150 mm³时，随机分为4组（每组n=6）：溶媒组（0.1% DMSO+生理盐水）、贝沙罗汀（Bexarotene，LGD-1069）单药组（100 mg/kg/天，口服灌胃）、多西他赛单药组（5 mg/kg/周，腹腔注射）、联合组（贝沙罗汀+多西他赛）。治疗21天后，联合组肿瘤体积减少最显著（78%，从850 mm³降至187 mm³），单药贝沙罗汀组减少42%，单药多西他赛组减少38%。肿瘤组织TUNEL实验显示，联合组凋亡细胞数增加5.2倍[2]
- 小鼠肺癌模型：
1. A/J小鼠（雌性，6-8周龄）腹腔注射100 mg/kg乌拉坦诱导肺肿瘤，4周后分为2组（每组n=10）：对照组（标准啮齿类饲料）、贝沙罗汀（Bexarotene，LGD-1069）组（饲料中掺入贝沙罗汀，按100 mg/kg体重/天给药，根据日均进食量计算）。喂养16周后安乐死小鼠，取肺组织用10%福尔马林固定，解剖显微镜下计数表面肿瘤数量和大小：贝沙罗汀组肺肿瘤数量减少52%（从18.3个/鼠降至8.8个/鼠），肿瘤体积减少45%（平均直径从1.2 mm降至0.66 mm）[3]
2. 携带皮下3LL肿瘤（200-250 mm³）的C57BL/6小鼠，口服贝沙罗汀（Bexarotene，LGD-1069）（50 mg/kg/天）持续14天，肿瘤体积减少48%（从920 mm³降至478 mm³），中位生存期延长30%（从26天延长至33.8天）[3]

RXR响应性荧光素酶报告基因实验：HEK293细胞以5×10⁴细胞/孔接种于24孔板，含10% FBS的DMEM培养24小时。用转染试剂共转染0.5 μg人RXRα/β/γ表达质粒、0.5 μg RXR响应性荧光素酶报告质粒（含DR1型RXR结合元件）和0.1 μg β-半乳糖苷酶质粒（内参）。转染24小时后，更换为含贝沙罗汀（Bexarotene，LGD-1069）（1、10、100、1000 nM）或溶媒（0.1% DMSO）的无血清DMEM，继续孵育24小时。用报告基因裂解缓冲液裂解细胞， luminometer检测荧光素酶活性，比色法检测β-半乳糖苷酶活性以校正转染效率，非线性回归计算EC50[1]

细胞增殖测定[2]
细胞类型：人 PCa 雄激素非依赖性细胞系 PC3 和 DU145
测试浓度：5、10、20、30 , PC3 细胞为 40 μM； DU145 细胞为 1、5、10、20、40 μM。
孵育持续时间：24和48小时
实验结果：证明具有抗增殖作用，IC50分别为40.62±0.45 µM (PC3)和50.20 ±4.10 µM (DU145)。

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细胞活力测定[2]
细胞类型： PC3 和 DU145 细胞
测试浓度： 20 和 40 µM
<孵化持续时间：24或48小时
实验结果：24小时处理后细胞周期蛋白D1和细胞周期蛋白E2减少。治疗 48 小时后，不仅减少了细胞周期蛋白 D1 和细胞周期蛋白 E2 的表达，而且抑制了细胞周期蛋白 B1 和 CDK1 的表达。

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前列腺癌细胞增殖与凋亡实验：
1. PC-3、LNCaP、DU145细胞分别以2×10³细胞/孔（PC-3/DU145）或3×10³细胞/孔（LNCaP）接种于96孔板，含10% FBS的RPMI 1640培养24小时。加入贝沙罗汀（Bexarotene，LGD-1069）（0.1-10 μM）单药或与多西他赛（1 nM）联合处理，孵育72小时。加入20 μL MTT（5 mg/mL），4小时后用DMSO溶解甲瓒结晶，570 nm处测吸光度计算细胞活力[2]
2. 凋亡检测：PC-3细胞以2×10⁵细胞/孔接种于6孔板，用贝沙罗汀（5 μM）+多西他赛（1 nM）处理48小时后裂解，使用荧光底物（Ac-DEVD-AMC）检测胱天蛋白酶-3/7活性，酶标仪检测荧光强度（激发380 nm，发射460 nm）[2]
- 肺癌细胞克隆形成实验：3LL和A549细胞以500细胞/孔接种于6孔板，培养24小时后加入贝沙罗汀（Bexarotene，LGD-1069）（0.5-20 μM），孵育14天（3LL）或18天（A549）形成集落。4%多聚甲醛固定，0.1%结晶紫染色，计数>50个细胞的集落，以溶媒对照组为基准计算抑制率[3]
- 细胞周期蛋白Western blot检测：3LL细胞（10 cm培养皿中2×10⁶细胞/皿）用5 μM 贝沙罗汀（Bexarotene，LGD-1069）处理48小时，含蛋白酶抑制剂的RIPA缓冲液裂解，BCA法测蛋白浓度。30 μg蛋白经10% SDS-PAGE电泳后转移至PVDF膜，一抗孵育p21、Cyclin D1和β-肌动蛋白（内参），HRP标记二抗结合后ECL显色，ImageJ定量条带灰度[3]

Animal/Disease Models: UL53-3 mice (p53wt/wtK-raswt/wt, p53val135/wtK-raswt/wt, or p53wt/wtK-rasko/wt)[3]
Doses: 100 mg/kg
Route of Administration: Gavage with 18 gage of gavage -needle, 0.1 mL per mouse per day, 5 times a week, continued for 12 weeks
Experimental Results: Inhibited both tumor multiplicity and tumor volume in mice of all three genotypes.

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Prostate Cancer Xenograft Model (PC-3): Male BALB/c nu/nu mice (6-8 weeks old, 20-22 g) were housed under SPF conditions (22±2°C, 12-hour light/dark cycle, free access to food/water). Mice were subcutaneously injected with 5×10⁶ PC-3 cells (suspended in 100 μL PBS + 50 μL Matrigel) into the right flank. When tumors reached 100-150 mm³, mice were randomized into 4 groups (n=6/group):
- Vehicle: 0.1% DMSO + normal saline, oral gavage once daily;
- Bexarotene (LGD-1069) alone: 100 mg/kg/day, dissolved in 0.1% DMSO + normal saline, oral gavage once daily;
- Docetaxel alone: 5 mg/kg/week, dissolved in normal saline, intraperitoneal injection once weekly;
- Combination: Bexarotene (100 mg/kg/day, oral) + docetaxel (5 mg/kg/week, ip).
Treatment lasted 21 days. Tumor volume was measured every 3 days (volume = length × width² / 2). On day 21, mice were euthanized, tumors were harvested for TUNEL assay, and serum was collected for cytokine analysis [2]
- Murine Lung Cancer Models:
1. A/J mouse urethane-induced lung tumor model: Female A/J mice (6-8 weeks old, 18-20 g) were intraperitoneally injected with 100 mg/kg urethane (dissolved in saline). Four weeks later, mice were divided into 2 groups (n=10/group): control (standard rodent diet) and Bexarotene (LGD-1069) (diet containing bexarotene at 100 mg/kg body weight/day, calculated based on average daily food intake). Mice were fed the respective diets for 16 weeks, then euthanized. Lungs were removed, fixed in 10% formalin, and the number and size of surface tumors were counted under a dissecting microscope [3]
2. C57BL/6 mouse 3LL xenograft model: Female C57BL/6 mice (6-8 weeks old) were subcutaneously injected with 1×10⁶ 3LL cells into the right flank. When tumors reached 200-250 mm³, mice were randomized into 2 groups (n=8/group): vehicle (0.5% carboxymethylcellulose sodium, CMC-Na, 10 mL/kg/day, oral gavage) and Bexarotene (LGD-1069) (50 mg/kg/day, dissolved in 0.5% CMC-Na, oral gavage). Treatment continued until mice met euthanasia criteria (tumor volume > 2000 mm³ or >15% weight loss). Survival time was recorded daily, and tumor volume was measured every 2 days [3]

Absorption, Distribution and Excretion
Bexarotine and its known metabolites have limited excretion pathways (<1% of the administered dose). After oral administration, bexarotine is absorbed, with a time to peak concentration (Tmax) of approximately two hours. …Studies in patients with advanced malignancies have shown that, within the therapeutic range, single-dose drug concentrations exhibit an approximately linear relationship, with lower accumulation after multiple doses. Compared to glucose solution, plasma AUC and Cmax values of 75–300 mg bexarotine increased by 35% and 48%, respectively, after ingestion of a fatty diet. Bexarotine has a high binding rate to plasma proteins (>99%). The plasma proteins bound to bexarotine are not yet fully understood, and the ability of bexarotine to displace drugs bound to plasma proteins and the ability of drugs to displace bexarotine bindings have not been investigated. Renal excretion of bexarotine and its metabolites was examined in patients with type 2 diabetes. Neither bexarotine nor its metabolites were excreted in large quantities in the urine. Bexarotine is believed to be primarily excreted via the hepatobiliary system.

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Metabolism/Metabolites
Four bexarotine metabolites have been identified in plasma: 6-hydroxybexarotine, 7-hydroxybexarotine, 6-oxobexarotine, and 7-oxobexarotine. In vitro studies have shown that cytochrome P450 3A4 is the major cytochrome P450 responsible for the formation of oxidative metabolites, and these oxidative metabolites may undergo glucuronidation. These oxidative metabolites are active in in vitro assays of retinoid receptor activation, but the relative contributions of the parent compound and its metabolites to the efficacy and safety of bexarotine are unclear.
Known human metabolites of bexarotine include 6-hydroxybexarotine, 7-hydroxybexarotine, and 7-oxobexarotine.

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Biological Half-Life
7 hours
The terminal half-life of bexarotine is approximately 7 hours.

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The oral bioavailability of bexarotine (LGD-1069) in rats is approximately 40%, and the oral bioavailability in humans is approximately 35%.After oral administration of 100 mg/kg to rats, the peak plasma concentration (Cmax) was 2.8 μg/mL, the time to peak concentration (Tmax) was 2 hours, and the elimination half-life (t1/2) was 7.5 hours. The drug is highly bound to plasma proteins (>99%) and distributed in various tissues, with the highest concentrations in the liver, adipose tissue, and skin (target tissues for cutaneous T-cell lymphoma)[1]. Metabolism: Bexarotine (LGD-1069) is mainly metabolized in the liver by cytochrome P450 enzymes (CYP3A4 and CYP2C8) to produce inactive metabolites, which are mainly excreted in feces (≈60%) and urine (≈30%) within 72 hours[1].

Hepatotoxicity
Approximately 5% of patients receiving bexarotine treatment experience elevated serum transaminases, but these abnormalities are usually mild, transient, and asymptomatic or without jaundice. However, there have been reports of clinically significant liver injury with jaundice caused by bexarotine treatment, some of which were severe and even fatal. Hepatotoxicity appears to be more common with high-dose treatment. The clinical characteristics of bexarotine-induced liver injury have not been described in detail, and no related case reports of hepatotoxicity have been published. However, the product label mentions hepatotoxicity and recommends regular monitoring of liver function. Probability Score: D (Possibly but uncommon, a cause of clinically significant liver injury).

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Protein Binding
>99% Interactions
Because bexarotine is metabolized by cytochrome P450 3A4, ketoconazole, itraconazole, erythromycin, gemfibrozil, grapefruit juice, and other cytochrome P450 3A4 inhibitors are expected to cause elevated plasma bexarotine concentrations. In addition, rifampin, phenytoin sodium, phenobarbital, and other cytochrome P450 3A4 inducers may lead to a decrease in plasma bexarotine concentrations.
Concomitant use of bexarotine capsules with gemfibrozil significantly increases plasma bexarotine concentrations, which may be at least partially related to gemfibrozil's inhibition of cytochrome P450 3A4. Under similar conditions, concomitant use of atorvastatin has no effect on bexarotine concentrations. Concomitant use of bexarotine capsules with gemfibrozil is not recommended.
According to interim data, concomitant use of bexarotine capsules with tamoxifen resulted in a decrease in plasma tamoxifen concentrations of approximately 35%, likely due to the induction of cytochrome P450 3A4. Based on this known interaction, bexarotine could theoretically increase the metabolic rate of other substrates metabolized by cytochrome P450 3A4 and decrease their plasma concentrations, including oral or other systemic hormonal contraceptives.
If bexarotine is treated concurrently or recently with drugs that cause blood disorders and these drugs also cause the same leukopenia and/or thrombocytopenia, the leukopenia and/or thrombocytopenia effect of bexarotine may be enhanced; if necessary, the dose of myelosuppressants should be adjusted according to blood cell counts.
For more complete data on interactions of bexarotine (of 10), please visit the HSDB record page.

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Preclinical toxicity in mice/rats:
-Oral administration of bexarotine (LGD-1069) (50-200 mg/kg) daily for 4 weeks caused dose-dependent adverse reactions: dry skin (occurring in 80% of mice at a dose of 100 mg/kg), hyperlipidemia (2.3-fold increase in triglycerides and 1.8-fold increase in cholesterol at a dose of 150 mg/kg), and mild hepatomegaly (10% increase in liver weight at a dose of 200 mg/kg). No significant nephrotoxicity (no change in serum BUN/creatinine) or bone marrow suppression (normal peripheral blood cell count) was observed [1]
- In the 3LL xenograft model [3], mice treated with 50 mg/kg/day bexarotine for 14 days showed mild weight loss (<5% of baseline) and transient skin scaling, which subsided after discontinuation of the drug; no histopathological changes in the liver/kidneys were detected [3]
- Clinical toxicity (summarized in reference [1]): Common adverse events in patients with cutaneous T-cell lymphoma (CTCL) include skin reactions (dry skin, pruritus, rash, 65-75%), dyslipidemia (hypertriglyceridemia, 50-60%; hypercholesterolemia, 30-40%) and headache (20-25%). Grade 3/4 toxicities (incidence <10%) include severe hypertriglyceridemia (requiring lipid-lowering drugs) and hepatotoxicity (transient elevation of ALT/AST) [1]

[1]. A review of the molecular design and biological activities of RXR agonists. Med Res Rev. 2019 Jul;39(4):1372-1397.

[2]. Synergistic effect of a retinoid X receptor-selective ligand bexarotene and docetaxel in prostate cancer. Onco Targets Ther. 2019 Sep 24;12:7877-7886.

[3]. Prevention of lung cancer progression by bexarotene in mouse models. Oncogene. 2006 Mar 2;25(9):1320-9.

Bexarotene is a retinoid drug belonging to the benzoic acid and naphthalene compounds. It is an anti-tumor drug. Bexarotin (Targretin) is an anti-tumor drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of cutaneous T-cell lymphoma. It has also been used to treat off-label diseases such as lung cancer, breast cancer, and Kaposi's sarcoma. Bexarotin is a retinoid drug. Bexarotin is a retinoid analog used to treat the cutaneous manifestation of cutaneous T-cell lymphoma (CTCL). Bexarotin treatment is associated with higher rates of elevated serum enzymes, but clinically significant acute liver injury can occur in rare cases. Bexarotin is a synthetic retinoid drug with potential anti-tumor, chemopreventive, teratogenic, and embryotoxic effects. Bexarotin selectively binds to and activates the retinoic acid X receptor (RXR), thereby inducing altered gene expression, leading to reduced cell differentiation and proliferation, apoptosis in certain cancer cell types, and tumor regression. (NCI04)
A ralcinolone agonist (RXR-binding ligand), a tetrahydronaphthalene derivative, and a retinoic acid X receptor antagonist for the treatment of cutaneous T-cell lymphoma.
Indications

Oral administration for the treatment of cutaneous manifestations of cutaneous T-cell lymphoma (CTCL) in patients who have failed at least one prior systemic therapy. It may also be used to treat cutaneous lesions in patients with early-stage (stage IA and IB) cutaneous T-cell lymphoma (CTCL), particularly in patients who have failed or whose disease persists, or who cannot tolerate other therapies.
FDA Label
Targretin capsules are indicated for the treatment of cutaneous manifestations of advanced cutaneous T-cell lymphoma (CTCL) in patients who have failed at least one systemic therapy.
Mechanism of Action

Besarrotin selectively binds to and activates retinoic acid X receptor subtypes. There are three subtypes of retinoic acid X receptors: RXR_α, RXR_β, and RXR_γ. The exact mechanism of action of bexarotin in treating cutaneous T-cell lymphoma (CTCL) is unclear, but the drug has been effective in all clinical stages of CTCL. Bexarotin selectively binds to and activates retinoic acid X receptor subtypes (RXRα, RXRβ, RXRγ). RXR can form heterodimers with various receptors, such as the retinoic acid receptor (RAR), vitamin D receptor, thyroid receptor, and peroxisome proliferation-activating receptor (PPAR). Upon activation, these receptors act as transcription factors, regulating gene expression that controls cell differentiation and proliferation. Bexarotin inhibits the growth of certain hematopoietic and squamous cell-derived tumor cell lines in vitro. In some animal models, it also induces tumor regression in vivo. The exact mechanism of action of bexarotin in treating cutaneous T-cell lymphoma (CTCL) is unclear.

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Therapeutic Use
Therapeutic Category: Antineoplastic Drugs
Bexarotin is indicated for the treatment of cutaneous manifestations of cutaneous T-cell lymphoma in patients who have failed at least one other prior systemic therapy. /US product label contains/

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Drug Warning
May cause harm to the fetus; animal studies have shown teratogenicity and embryolethality. There are currently no adequate and well-controlled clinical studies. Pregnancy should be avoided during treatment. If used during pregnancy, the pregnant woman should be informed of the potential fetal risks. …Male patients receiving this drug should use condoms when having sexual intercourse with a pregnant or potentially pregnant woman.
Effective contraception must be used for one month before starting treatment, during treatment, and for at least one month after discontinuation; unless abstinence is chosen, it is recommended to use two reliable methods of contraception simultaneously. Bexarotine may induce metabolic enzymes, thereby theoretically reducing the plasma concentration of oral or other systemic hormonal contraceptives. In phase II-III clinical studies, 79% of patients receiving oral bexarotine developed hyperlipidemia. More than half of patients receiving 300 mg/m² or higher doses of bexarotine experienced elevated fasting triglycerides and cholesterol, and decreased high-density lipoprotein cholesterol. Lipid abnormalities usually appear within 2–4 weeks and are reversible upon discontinuation of the drug. If fasting triglycerides are elevated or elevated during treatment, lipid-lowering therapy should be initiated, and bexarotine should be reduced or discontinued. Acute pancreatitis has been reported in some patients receiving bexarotine, with at least one death. The manufacturer notes that patients with cutaneous T-cell lymphoma (CTCL) and risk factors for pancreatitis (e.g., a history of pancreatitis, uncontrolled hyperlipidemia, excessive alcohol consumption, uncontrolled diabetes, biliary tract disease, or use of medications associated with pancreatic toxicity or known to increase triglyceride levels) should generally not receive bexarotine. For more complete data on bexarotine (15 total), please visit the HSDB records page. Pharmacodynamics: Bexarotine belongs to the retinoid subclass that selectively activates retinoic acid X receptors (RXR). These retinoic acid receptors have different biological activity than retinoic acid receptors (RAR). Bexarotine is indicated for the treatment of cutaneous manifestations in patients with cutaneous T-cell lymphoma who have failed at least one prior systemic therapy. Bexarotine selectively binds to and activates retinoic acid X receptor subtypes (RXRα, RXRβ, RXRγ). RXR can form heterodimers with various receptors, such as the retinoic acid receptor (RAR), vitamin D receptor, thyroid receptor, and peroxisome proliferation-activating receptor (PPAR). Upon activation, these receptors act as transcription factors, regulating the expression of genes controlling cell differentiation and proliferation. Bexarotine inhibits the growth of certain hematopoietic and squamous cell-derived tumor cell lines in vitro. It can also induce tumor regression in vivo in some animal models. Mechanism of action: Bexarotine (LGD-1069) activates RXR, which can form homodimers or heterodimers with other nuclear receptors (e.g., PPARγ, LXRα). The activated RXR dimer binds to specific DNA response elements (e.g., DR1, DR5) in the promoters of target genes, regulating the transcription of genes involved in cell cycle arrest (e.g., p21), apoptosis (e.g., Bax), and lipid metabolism (e.g., ABCA1) [1,3]. Therapeutic applications: Bexarotin (LGD-1069) has been approved by the FDA for the treatment of patients with stage IIB-IV refractory cutaneous T-cell lymphoma (CTCL). Preclinical studies [2,3] support its potential in other cancers (prostate cancer, lung cancer), when used in combination with chemotherapeutic agents (e.g., docetaxel) or as a chemopreventive agent [1,2,3]
- Synergistic mechanism with docetaxel [2]:Bexarotin (LGD-1069) downregulated the expression of ABCB1 (a multidrug resistance pump) in PC-3 cells by 45%, thereby reducing docetaxel efflux and increasing intracellular drug accumulation. It can also enhance docetaxel-induced G2/M phase cell cycle arrest by upregulating p21 (from 32% to 58% in PC-3 cells) [2]
- Chemoprophylaxis of lung cancer [3]: Bexarotin (LGD-1069) inhibits lung tumor progression by reducing the enrichment of cancer stem cells (CSCs): it reduces the percentage of CD133⁺ CSCs in 3LL tumors from 12% to 4% and downregulates the expression of CSC-related genes (such as SOX2, Nanog) by 50-60% [3]

C24H28O2

348

348.208

153559-49-0

Bexarotene-d4;2182068-00-2

82146

White to off-white solid powder

1.0±0.1 g/cm3

489.7±44.0 °C at 760 mmHg

230-231ºC

229.5±23.1 °C

0.0±1.3 mmHg at 25°C

1.556

8.55

37.3

1

2

3

26

551

0

NAVMQTYZDKMPEU-UHFFFAOYSA-N

InChI=1S/C24H28O2/c1-15-13-20-21(24(5,6)12-11-23(20,3)4)14-19(15)16(2)17-7-9-18(10-8-17)22(25)26/h7-10,13-14H,2,11-12H2,1,3-6H3,(H,25,26)

4-[1-(3,5,5,8,8-pentamethyl-6,7-dihydronaphthalen-2-yl)ethenyl]benzoic acid

LGD1069; LGD 1069; LG 100069; Ro26-445; LGD-1069; SR-11247; Ro 26 445; Targretin Ro 26-445; SR 11247; SR11247; 3-methyl TTNEB. Bexarotene; US trade name: Targretin.

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)

配方 1 中的溶解度: 2.62 mg/mL (7.52 mM) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (这些助溶剂从左到右依次添加，逐一添加), 悬浮液；超声助溶。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: 2.62 mg/mL (7.52 mM) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (5.97 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清的DMSO储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 4 中的溶解度: ≥ 2.08 mg/mL (5.97 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100μL 20.8mg/mL澄清的DMSO储备液加入到900μL 20％SBE-β-CD生理盐水中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 5 中的溶解度: ≥ 2.08 mg/mL (5.97 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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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。