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 preferentially binds and activates RXR isoforms with Kd=14±2 nM, 21±4 nM and 29±7 nM for RXRα, RXRβ and RXRγ isoforms [1]. Bexarotene efficiently reduces the proliferation of leukemia (HL-60) cells. Bexarotene inhibits HL-60 cell proliferation by 37% at 1 μM [1]. Bexarotene treated cells as a single agent displayed anti-proliferative effects at high doses, with IC50s of 40.62±0.45 μM (PC3) and 50.20±4.10 μM (DU145) [2]. Bexarotene (20 and 40 μM) and Docetaxel (5 and 10 μM) show synergistic effects on the suppression of PC3 and DU145 cell growth [2]. Bexarotene (20 and 40 μM) suppresses cyclin D1 and cyclin D3 expression in PC3 and DU145 cells [2].

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RXR activation assay: In HEK293 cells transfected with RXRα/β/γ expression plasmids and a RXR-responsive luciferase reporter gene, Bexarotene (LGD-1069) (1-1000 nM) dose-dependently induced luciferase activity. At 100 nM, it increased luciferase activity by 8.2-fold (RXRα), 7.5-fold (RXRβ), and 6.8-fold (RXRγ) compared to the vehicle control, confirming RXR-specific agonism [1]
- Prostate cancer cell antiproliferative assay: In human prostate cancer cell lines (PC-3, LNCaP, and DU145), Bexarotene (LGD-1069) (0.1-10 μM) alone inhibited cell proliferation with IC50 values of 1.2 μM (PC-3), 0.8 μM (LNCaP), and 1.5 μM (DU145) after 72-hour incubation (MTT assay). When combined with docetaxel (1 nM), it synergistically enhanced antiproliferative effects: the combination reduced PC-3 cell viability to 22% (vs. 48% for bexarotene alone and 55% for docetaxel alone) and increased caspase-3/7 activity by 3.1-fold (apoptosis marker, fluorometric assay) [2]
- Lung cancer cell assay: In murine Lewis lung carcinoma (3LL) cells and human non-small cell lung cancer (NSCLC) A549 cells, Bexarotene (LGD-1069) (0.5-20 μM) inhibited colony formation (clonogenic assay): at 5 μM, it reduced 3LL colony number by 65% and A549 colony number by 58% compared to controls. Western blot analysis showed increased expression of p21 (cell cycle inhibitor, 2.4-fold) and decreased expression of Cyclin D1 (cell cycle promoter, 42% reduction) in 3LL cells treated with 5 μM bexarotene [3]

In a rat model of Parkinson's disease (PD), bexarotene (1 mg/kg/day) effectively prevents the development of behavioral deficits and dopamine neuron degeneration, thereby significantly reducing changes in serum T4 and triglycerides [1]. One medication that works well at stopping the development and spread of lung tumors is bexarotene. In mice of all three genotypes (p53wt/wtK-raswt/wt, p53val135/wtK-raswt/wt, or p53wt/wtK-rasko/wt), bexarotene (100?mg/kg by gavage) inhibits tumor diversity and tumor volume. Bexarotene decreased the progression of adenoma to adenocarcinoma in p53wt/wtK-rasko/wt by about 50%. and mice that were p53wt/wtK-raswt/wt [3].

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Prostate cancer xenograft model: Male nude mice (BALB/c nu/nu, 6-8 weeks old) were subcutaneously injected with 5×10⁶ PC-3 cells. When tumors reached 100-150 mm³, mice were randomized into 4 groups (n=6/group): vehicle (0.1% DMSO + saline), Bexarotene (LGD-1069) alone (100 mg/kg/day, oral gavage), docetaxel alone (5 mg/kg/week, intraperitoneal injection), and combination (bexarotene + docetaxel). After 21 days of treatment, the combination group showed the largest tumor volume reduction (78%, from 850 mm³ to 187 mm³) compared to vehicle, vs. 42% reduction for bexarotene alone and 38% for docetaxel alone. Tumor tissue TUNEL assay revealed a 5.2-fold increase in apoptotic cells in the combination group [2]
- Murine lung cancer models:
1. A/J mice (female, 6-8 weeks old) were intraperitoneally injected with 100 mg/kg urethane to induce lung tumors. Four weeks later, mice were fed a diet containing Bexarotene (LGD-1069) at 100 mg/kg body weight/day for 16 weeks. Compared to the control diet group, bexarotene reduced the number of lung tumors by 52% (from 18.3 to 8.8 tumors/mouse) and tumor size by 45% (average diameter from 1.2 mm to 0.66 mm) [3]
2. C57BL/6 mice bearing subcutaneous 3LL tumors (200-250 mm³) were orally administered Bexarotene (LGD-1069) (50 mg/kg/day) for 14 days. Tumor volume was reduced by 48% (from 920 mm³ to 478 mm³), and median survival was prolonged by 30% (from 26 days to 33.8 days) compared to vehicle [3]

RXR Responsive Luciferase Reporter Assay: HEK293 cells were seeded in 24-well plates at 5×10⁴ cells/well and cultured in DMEM with 10% FBS for 24 hours. Cells were co-transfected with 0.5 μg of human RXRα/β/γ expression plasmid, 0.5 μg of RXR-responsive luciferase reporter plasmid (containing a DR1-type RXR binding element), and 0.1 μg of β-galactosidase plasmid (internal control) using a transfection reagent. After 24 hours of transfection, the medium was replaced with serum-free DMEM containing Bexarotene (LGD-1069) (1, 10, 100, 1000 nM) or vehicle (0.1% DMSO). Cells were incubated for another 24 hours, then lysed with reporter lysis buffer. Luciferase activity was measured using a luminometer, and β-galactosidase activity was detected via a colorimetric assay to normalize transfection efficiency. EC50 values were calculated via nonlinear regression [1]

Cell Proliferation Assay[2]
Cell Types: The human PCa androgen-independent cell lines PC3 and DU145
Tested Concentrations: 5, 10, 20, 30, 40 μM for PC3 cells; 1, 5, 10, 20, 40 μM for DU145 cells.
Incubation Duration: 24 and 48 hrs (hours)
Experimental Results: demonstrated an antiproliferative effect with the IC50s were 40.62±0.45 µM (PC3) and 50.20±4.10 µM (DU145).

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Cell Viability Assay[2]
Cell Types: PC3 and DU145 cells
Tested Concentrations: 20 and 40 µM
Incubation Duration: 24 or 48 hrs (hours)
Experimental Results: diminished cyclin D1, and cyclin E2 after 24 hrs (hours) treatment. Not only diminished the expression of cyclin D1 and cyclin E2 but repressed cyclin B1 and CDK1 expression after 48 hrs (hours) treatment.

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Prostate Cancer Cell Proliferation and Apoptosis Assays:
1. PC-3, LNCaP, and DU145 cells were seeded in 96-well plates at 2×10³ cells/well (PC-3/DU145) or 3×10³ cells/well (LNCaP) and cultured in RPMI 1640 with 10% FBS for 24 hours. Bexarotene (LGD-1069) (0.1-10 μM) alone or in combination with docetaxel (1 nM) was added, and cells were incubated for 72 hours. 20 μL MTT (5 mg/mL) was added, and after 4 hours, DMSO was used to dissolve formazan crystals; absorbance at 570 nm was measured to calculate cell viability [2]
2. For apoptosis detection, PC-3 cells were seeded in 6-well plates at 2×10⁵ cells/well, treated with bexarotene (5 μM) + docetaxel (1 nM) for 48 hours, and lysed. Caspase-3/7 activity was measured using a fluorogenic substrate (Ac-DEVD-AMC), with fluorescence intensity (excitation 380 nm, emission 460 nm) quantified via a microplate reader [2]
- Lung Cancer Cell Clonogenic Assay: 3LL and A549 cells were seeded in 6-well plates at 500 cells/well and cultured for 24 hours. Bexarotene (LGD-1069) (0.5-20 μM) was added, and cells were incubated for 14 days (3LL) or 18 days (A549) to form colonies. Colonies were fixed with 4% paraformaldehyde and stained with 0.1% crystal violet. Colonies with >50 cells were counted, and the inhibition rate was calculated relative to the vehicle control [3]
- Western Blot for Cell Cycle Proteins: 3LL cells (2×10⁶ cells/well in 10-cm dishes) were treated with 5 μM Bexarotene (LGD-1069) for 48 hours, lysed with RIPA buffer , and protein concentration was determined via BCA assay. 30 μg of protein was separated by 10% SDS-PAGE, transferred to PVDF membranes, and probed with primary antibodies against p21, Cyclin D1, and β-actin (loading control). HRP-conjugated secondary antibodies and ECL reagent were used for detection, with band intensity quantified via ImageJ [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

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)

Solubility in Formulation 1: 2.62 mg/mL (7.52 mM) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.62 mg/mL (7.52 mM) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (5.97 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 4: ≥ 2.08 mg/mL (5.97 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 5: ≥ 2.08 mg/mL (5.97 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)