TLC-2716 (4℃, 1 hour) bound to recombinant human LXRα (EC50 = 7 nM) and LXRβ (EC50 = 15 nM) in biochemical binding assays [1]. TLC-2716 (16 hours) induced NCOR recruitment to LXRα and LXRβ in HEK293 mammalian two-hybrid assays, with EC50 values of 8 nM and 11 nM, respectively; and inhibited the activity of ABCA1 and SREBP1c reporter genes in HT-29 and HepG2 cells, respectively, with IC50 values of 15 nM and 7 nM, respectively [1]. TLC-2716 (5 days) reduced the accumulation of triglycerides in primary human Upcyte hepatocytes in a dose-dependent manner, with an EC50 value of 289 nM [1]. In fatty liver organoids, TLC-2716 (500 nM-5 μM; 3 days) dose-dependently reduced intracellular lipid content and inhibited the expression of LXR-related genes, lipid metabolism genes, inflammation genes and fibrosis-related genes, with enhanced effects in GCKRTT organoids [1].

TLC-2716 (0.3-1 mg/kg; gavage; once daily; for 3 weeks) dose-dependently improves dyslipidemia in high-fat diet-induced obese mice by reducing hepatic de novo lipogenesis, hepatic triglyceride (TG) content, and plasma TG and total cholesterol (TC) levels without affecting peripheral reverse cholesterol transport [1]. TLC-2716 (0.1-15 mg/kg; oral; once daily) reduces dyslipidemia-related endpoints and improves glucose homeostasis in ZDF rats without impairing liver function [1]. TLC-2716 (0.1-1 mg/kg; oral; once daily; for 21 days) reduces hepatic de novo lipogenesis (DNL) gene expression, hepatic TG, and plasma TG and TC levels in high-fat diet-fed SD rats without impairing liver function [1]. TLC-2716 (1 mg/kg; orally; once daily; for 8 days) reduced the expression of lipid metabolism genes in the liver of human liver chimeric mice and showed a trend toward reducing liver triglyceride (TG) levels [1]. TLC-2716 (15-120 mg/kg; orally; once daily; for 26 weeks) reduced plasma TG and total cholesterol (TC) levels in lean CD-1 mice without significant adverse effects [1]. TLC-2716 (1-15 mg/kg; orally; once daily; for 28 days) reduced plasma TG and TC levels in cynomolgus monkeys without significant adverse effects [1].

Animal/Disease Models:C57BL/6 (male, 18 weeks old, obesity induced by a 14-week high-fat diet) [1]
Doses: 0.3 mg/kg; 1 mg/kg
Route of Administration: Oral; once daily; for 21 days
Experimental Results: The expression of de novo lipogenesis (DNL) genes in the liver, including Scd1, Fasn, Srebp1c, and Acaca, was reduced in a dose-dependent manner. The liver triglyceride (TG) content and the area under the curve (AUC) values of plasma TG and total cholesterol (TC) were reduced in the 1 mg/kg dose group, while the reduction was smaller in the 0.3 mg/kg dose group. Plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were comparable to those in the solvent control group. Ileal Srebp1c expression was downregulated in a dose-dependent manner.

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Animal/Disease Models:Zucker diabetic obese mice (ZDF) (male, 6-7 weeks old, obese fa/fa) [1]
Doses: 0.1 mg/kg; 1 mg/kg; 15 mg/kg
Route of Administration: Oral; once daily; 14 days (0.1, 1 mg/kg); Oral; once daily; 28 days (15 mg/kg)
Experimental Results: Hepatic DNL gene expression, hepatic TG content, and plasma TG and TC AUC were all decreased in the 0.1 and 1 mg/kg dose groups. Fasting blood glucose was reduced by about 56% in the 15 mg/kg dose group, and hepatic Angptl3 expression and plasma ANGPTL3 levels were decreased. Plasma ALT and AST levels were unchanged compared with the control group.

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Animal/Disease Models:Sprague-Dawley (SD) mice (male, 6-7 weeks old, high-fat diet induced obesity)[1]
Doses: 0.1 mg/kg; 1 mg/kg
Route of Administration: Oral; once daily; for 21 days
Experimental Results: Both doses reduced hepatic DNL gene expression, hepatic TG content, and plasma TG and TC AUC. Plasma ALT and AST levels remained unchanged compared to the solvent.

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Animal/Disease Models:PXB (male, humanized liver chimera) [1]
Doses: 1 mg/kg
Route of Administration: Gavage; once daily for 8 days
Experimental Results: The content of liver triglycerides showed a decreasing trend. The expression of liver cholesterol synthesis gene HMGCR, lipid clearance gene ANGPTL3, and de novo lipogenesis genes SREBP1C, FASN, ACACA, and SCD1 were all reduced.

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Animal/Disease Models:CD-1 (male and female, lean)[1]
Doses: 15 mg/kg; 60 mg/kg; 120 mg/kg
Route of Administration: Oral; Daily; 182 days
Experimental Results: All doses reduced plasma triglyceride (TG) and total cholesterol (TC) levels in both male and female mice. No adverse clinical manifestations, changes in liver biochemistry, or histopathological signs of liver injury were observed at any dose.

[1]. An oral, liver-restricted LXR inverse agonist for dyslipidemia: preclinical development and phase 1 trial. Nat Med. 2026;32(3):883-893.

C38H22CLF3N4O5S

739.12

Typically exists as solids at room temperature

OC(CNC(C1=CC=C(C2=CC(C3=C(C4=C(C#N)C=CC=C4C#N)C5=CC(F)=CC=C5N3S(C6=CC=C(C(F)F)C=C6)(=O)=O)=CC=C2)C(Cl)=C1)=O)=O

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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