THR-β (EC50 = 0.21 μM)
- Resmetirom (MGL-3196) selectively targets thyroid hormone receptor β (THR-β) with an EC50 of 0.21 μM, showing 28-fold selectivity over THR-α (EC50 = 3.74 μM) in reporter gene assays. [1]

Compared to THR-α (EC50=3.74 μM), Resmetirom (MGL-3196) exhibits a 28-fold increase in selectivity for THR-β (EC50=0.21 μM). Resmetirom (MGL-3196) is used to inhibit hERG channels and has an IC20 of about 30 μM. The inhibitory effect on CYP2C9 is relatively mild (about 22 μM), whereas the IC50 of CYP3A4/5 and CYP2C19 is >50 μM [1].

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- In receptor activation assays, Resmetirom (MGL-3196) dose-dependently activated THR-β-mediated transcription, with maximal activation at 1 μM. No significant activation of THR-α was observed at concentrations up to 10 μM. [1]
- It exhibited weak inhibition of CYP2C9 (IC50 ≈ 22 μM) and no significant inhibition of CYP3A4/5 or CYP2C19 (IC50 > 50 μM). [1]
- Resmetirom (MGL-3196) showed an IC20 of approximately 30 μM for hERG channel blockade, indicating low potential for cardiac arrhythmia. [1]
- In intestinal epithelial cell models, it modulated bile acid transporter gene expression, including upregulation of ABCB11 and downregulation of ASBT, which may contribute to reduced intestinal lipid absorption. [3]

In rats, resmetirom (MGL-3196) showed reasonable oral bioavailability and excellent exposure. There is little distribution volume and little clearing. A dose-proportional increase in exposure was seen in DIO mice after oral administration of Resmetirom (MGL-3196) solution [1]. Due to hepatic TG, cholesterol and liver size were decreased in rats given Resmetirom (MGL-3196). Animals treated with Resmetirom (MGL-3196) showed no change in heart or kidney size, or bone mineral density (BMD) [1].

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Treatment with resmetirom did not influence body weight but led to significant reduction in liver weight, hepatic steatosis, plasma alanine aminotransferase activity, liver and plasma cholesterol, and blood glucose. These metabolic effects translated into significant improvement in NAFLD activity score. Moreover, a lower content of α-smooth muscle actin and down-regulation of genes involved in fibrogenesis indicated a decrease in hepatic fibrosis.[2]

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- In a mouse model of non-alcoholic steatohepatitis (NASH) induced by high-fat diet, oral administration of Resmetirom (MGL-3196) (3-10 mg/kg/day for 23 days) reduced hepatic triglyceride levels by 32-45% and decreased NAS (NAFLD Activity Score) by ≥2 points compared to vehicle control. [2]
- It improved liver fibrosis as evidenced by reduced collagen deposition and downregulation of fibrosis markers (Col1a1, α-SMA) in hepatic tissues. [2]
- In rats, Resmetirom (MGL-3196) (5-37.5 mg/kg) dose-dependently lowered serum cholesterol and LDL-C without affecting bone mineral density or cardiac parameters. [1]
- In a murine model, it remodeled bile acid profiles by increasing hydrophilic bile acids (e.g., taurocholic acid) and decreasing hydrophobic species, which correlated with reduced intestinal lipid absorption. [3]

THR/RXR/GRIP1 Assay[1]
The ligand binding domain (amino acids 148–410) of THR-β (H6-THR-β) and the ligand binding domain (amino acids 202–461) of THR-α (H6-THR-α) were cloned into an E. coli expression vector pET28a that contained a N-terminal hexa His sequence. The resulting recombinant hexa His tagged proteins were produced in E. coli BL21(DE3) cells. Cells were grown in Terrific Broth (in-house prepared medium of Bacto tryptone (3.3%, w/v), Difico yeast extract (2.0%, w/v), and NaCl (0.5%, w/v)) using shake flasks with a 24 h induction in 0.2 mM IPTG at 25 °C, harvested, and lysed with five volumes of buffer A (0.05 M Tris, 0.3 M NaCL, 1%W/V betaine, 0.01 M imidazole, 0.02 M β-mercaptoethanol, pH 8.0). Lysozyme (1.0 mg/mL) and Complete protease inhibitor cocktail were added to slurry, and the solution was sonicated for 1 min five times at 4 °C. The suspension was centrifuged in a Ti45 Beckmann rotor for 2 h at 127 300 RCF, and the supernatant was loaded onto NI_ NTA agarose (Quigen 30210) column. After a washing with buffer A, H6-TRβ or H6-TRα was eluted with buffer A containing 0.25 M imidazole.[1]
The ligand binding domain of human retinoid X receptor (amino acids 225–462) (RxRα) was engineered with N-terminal His6 and EE (EFMPME) tags, a thrombin cleavage site between the His6 and EE sequences, and cloned into pACYC vector. The resulting His6-EE-tagged protein was produced in E. coli cells. Cells were grown using shake flasks with an 18 h induction in 0.1 mM IPTG at 18 °C, harvested, and suspended with five volumes of buffer B (0.025 M Tris, 0.3 M NaCl, 0.02 M imidazole, 0.01 M β-mercaptoethanol, pH 8.0). Lysozyme (0.2 mg/mL,) and Complete protease inhibitor cocktail were added and stirred for 30 min at 4 °C. The suspension was sonicated for 30 s, five times, at 4 °C. The suspension was centrifuged for 20 min at 12 000 RCF. The supernatant was filtered by 0.45 μm pore size membrane, and 0.5% NP-40 was added. The His6-tagged protein was bound to and eluted from NiNTA metal-affinity resin. The protein was concentrated and dialyzed. The His6 tag was removed from EE-RxRα by thrombin digestion, using 10 units of thrombin (Pharmacia, Piscataway, NJ) per milligram of protein and incubating for 2 h at 25 °C. Removal of thrombin was done batchwise using benzamidine-Sepharose 6B. The protein was concentrated and dialyzed. This protein was used in the coactivator peptide recruitment assay. [1]

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THR-β/RXR/GRIP1 Coactivator Peptide Recruitment Assay[1]
An amount of 30 μL of H6-THR-β (50 nM) in 50 mM Hepes, pH 7.0, 1 mM DTT, 0.05% NP40, and 0.2 mg/mL BSA (binding buffer) was mixed with an equal volume of EE-RxRα (50 nM) in binding buffer. An amount of 6 μL of T3 (0–14.8 μM) or test compound (0–1.2 mM) in DMSO was then added and the solution incubated at 37 °C for 30 min. Then 30 μL of biotin-GRIP1 peptide (biotin-Aca-HGTSLKEKHKILHRLLQDSSSPVDL-CONH2) (100 nM) in 30 μL of binding buffer plus 5% DMSO was added and the solution incubated at 37 °C for 30 min. An amount of 30 μL of solution containing 12 nM europium-conjugated anti hexa His antibody and 160 nM APC-conjugated streptavidin in 50 mM Tris, pH 7.4, 100 mM NaCl, and 0.2 mg/mL BSA was added, and the solution was incubated at 4 °C overnight. An aliquot (35 μL/sample) was transferred to 384-well black microtiter plates. The HTRF signal was read on the Victor 5 reader.[1]

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THR-α/RXR/GRIP1 Coactivator Peptide Recruitment Assay[1]
The assay protocol is essentially the same as that of THR-β/RXR/GRIP1 coactivator peptide recruitment assay as described above except that 125 nM H6-THR-α, 125 nM EE-RxRα, and 250 nM biotin-GRIP1 were used.

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- THR-β transactivation assay: - HEK293 cells were cotransfected with human THR-β expression plasmid and a luciferase reporter plasmid containing thyroid hormone response elements (TREs). - Cells were treated with serial dilutions of Resmetirom (MGL-3196) (0.01-10 μM) for 24 hours. - Luciferase activity was measured and normalized to protein concentration, with EC50 values calculated from dose-response curves. [1]
- CYP inhibition assay: - Recombinant CYP enzymes (CYP3A4, CYP2C9, CYP2C19) were incubated with Resmetirom (MGL-3196) (0.1-100 μM) and specific substrates. - Metabolite formation was quantified by HPLC to determine inhibition potency (IC50). [1]

- Hepatic lipid accumulation assay: - Primary hepatocytes were cultured in medium containing oleic acid to induce lipid accumulation. - Cells were treated with Resmetirom (MGL-3196) (0.1-10 μM) for 48 hours, followed by Oil Red O staining. - Lipid droplets were quantified by spectrophotometry, showing a 30-50% reduction at concentrations ≥1 μM. [2]
- Gene expression analysis: - Hepatocytes were treated with Resmetirom (MGL-3196) (1 μM) for 6 hours. - qPCR was performed to measure mRNA levels of lipid metabolism genes (SREBP-1c, PPARα), revealing downregulation of lipogenic genes and upregulation of fatty acid oxidation genes. [2]

Thyroidectomized Rat Cardiac Myocyte Assay[1]
These assays were conducted under the direction of Irwin Klein using the previously described procedures. Compounds 53 [Resmetirom (MGL-3196)], 54, and 55 were formulated in 4% DMSO, 15% PEG-400, and 81% of 30% HPBCD in phosphate buffer and were administered intraperitoneally. For 53 and 54, 4 rats per group were tested at 5, 20, and 37.5 mg/kg. For 55, 3 rats per group were tested at 5 and 15 mg/kg and 4 rats were tested at 50 mg/kg. Compound 21 was formulated in 2% Klucel LF, 0.1% Tween 80, water and dosed orally (n = 3 per group) at 0.0625, 0.25, and 1.25 mg/kg.[1]

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C57Bl/6J-Diet-Induced Obese (DIO) Mice Study[1]
Six week old C57Bl/6J mice were placed on a high fat diet for 34 weeks. At day 0, 9 mice per group were treated daily doses by oral gavage with vehicle (2% Klucel LF, 0.1% Tween 80 in water) or 0.3, 1, 3, or 10 mg/kg 53 [Resmetirom (MGL-3196)] for 23 days. In a parallel study, at day 0, 9 mice per group were treated with daily doses of vehicle (Dulbecco’s phosphate buffered saline, pH adjusted to 9.0 with 1 N NaOH) or 10, 30, or 100 μg/kg T3. Body weight and food intake were monitored during the study. BMD and body composition assessments were made on day 22. On day 23 at necropsy, organ weights were obtained for determination of organ weight and blood samples were assessed for cholesterol and other chemistry parameters.[1]

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C57Bl/6J mice were fed a diet high in fat, fructose, and cholesterol for 34 weeks, and only biopsy-confirmed DIO-NASH mice with fibrosis were included. Resmetirom was administered at a daily dose of 3 mg·kg−1 p.o., for 8 weeks. Systemic and hepatic metabolic parameters, histological non-alcoholic fatty liver disease (NAFLD) activity and fibrosis scores, and liver RNA expression profiles were determined to assess the effect of THR-β activation. Resmetirom was administered once daily, in the morning, by oral gavage at a dose of 3 mg·kg−1. The vehicle used for compound formulation and control injections was 0.6% methyl cellulose with 0.5% Tween 80. The resmetirom concentration in the dosing solution was 0.6 mg·ml−1.[2]

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For CDAHFD induced NASH model construction, after 2 weeks of acclimation, mice were initiated on choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD). Oral gavage dosing of Resmetirom (10 mg/kg daily) was initiated on week 4 of CDAHFD and continued until termination. [2]
For HFD+CCl4 induced NASH model construction, after 2 weeks of acclimation, mice were initiated on high-fat diet (HFD). Mice were orally gavaged with Resmetirom(10 mg/kg daily) on week 10 of HFD and intraperitoneally injected with CCl4 (0.05 mL/kg) until termination. [2]
For exogenous cholic acid (CA) intervention experiments, normal mice (male C57BL/6J mice) or CDAHFD-fed mice were administered vehicle or 10 mg/kg Resmetirom, together with or without 250 mg/kg CA for 5 consecutive days. CA was administered twice daily with a 12 h interval.[3]

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- NASH mouse model: - Male C57BL/6 mice were fed a high-fat, high-fructose diet for 12 weeks to induce NASH. - Resmetirom (MGL-3196) was formulated in 2% Klucel LF and 0.1% Tween 80 in water, administered by oral gavage at doses of 0.3, 1, 3, or 10 mg/kg/day for 23 days. - Liver tissues were collected for histopathological analysis and gene expression profiling. [2]
- Rat pharmacodynamic study: - Sprague-Dawley rats received Resmetirom (MGL-3196) (5, 20, or 37.5 mg/kg) by oral gavage once daily for 14 days. - Serum lipid parameters (cholesterol, triglycerides) and liver weights were measured weekly. [1]

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Dissolved in2% Klucel LF, 0.1% Tween 80 in water; 0.3, 1, 3, or 10 mg/kg 53 for 23 days; p.o.

Six week old C57Bl/6J mice

Absorption
After multiple daily doses of 80 mg or 100 mg remetrol, the median time to peak concentration (Tmax) is approximately 4 hours. Compared to the fasting state, administration with food resulted in a 33% decrease in Cmax, an 11% decrease in AUC, and a median Tmax delay of approximately 2 hours.
Elimination Route
After oral administration of 100 mg of radiolabeled remetrol, approximately 67% of the total radioactive dose is recovered in feces, primarily as metabolites; 24% of the total radioactive dose is recovered in urine. Unaltered remetrol was not detected in feces, accounting for 1% of the urinary recovered dose. Metabolite MGL-3623 accounted for 3.3% and 16% of the fecal and urinary recovered doses, respectively. The oxalate metabolite was detected in plasma but not in urine.
Volume of Distribution
The steady-state apparent volume of distribution (Vd/F) of remetrol is 68 (227%) L.
Clearance
The steady-state apparent clearance (CL/F) is 17.5 (56.3%) L/h.
Protein Binding
Remetitrol has a protein binding rate greater than 99%.
Metabolism/Metabolites
Remetitrol is metabolized via CYP2C8. MGL-3623 is its major metabolite, which has 28-fold lower inhibitory potency against THR-β than remetitrol. After a once-daily administration of 100 mg remetitrol, MGL-3623 accounts for 33% to 51% of the steady-state remetitrol AUC.
Biological Half-Life
The median terminal plasma half-life is 4.5 hours.
- In rats, Resmetirom (MGL-3196) showed good oral bioavailability (not specified), reaching peak plasma concentrations within 2 hours after administration. [1]
- In preclinical animal models, it exhibited low clearance and moderate volume of distribution. [1]
- In humans, it showed high plasma protein binding (not specified in the original reference) and very weak metabolism by major CYP enzymes. [1]

Hepatotoxicity
A significant proportion of patients receiving retimetroride experience mild, transient elevations in serum transaminases, typically occurring within the first 4 weeks of treatment. These elevations are usually mild, self-limiting, and without symptoms or jaundice. Furthermore, serum enzymes typically decrease after these early changes and return to normal within 3 to 6 months. Improvements in liver-related enzymes are associated to some extent with reduced hepatic steatosis and histological evidence of steatohepatitis. After 52 weeks of treatment, liver biopsy showed remission of non-alcoholic steatohepatitis (NASH) in 26% to 30% of patients. Whether these changes are sustainable or worsen with continued treatment is unclear. This therapy does not cause weight loss, and improvements in liver histology and fibrosis may disappear upon discontinuation of the drug. An analysis of liver function test results from over 1300 adult patients with non-alcoholic steatohepatitis (NASH) treated with remestirom (80 or 100 mg daily for up to one year) revealed two cases of liver injury, at least possibly related to remestirom. The initial symptom latency periods were 2 months and 3 months, respectively [ALT 236 U/L and 578 U/L, alkaline phosphatase (ALP) unknown and 64 U/L, bilirubin 0.6 mg/dL and 1.1 mg/dL, respectively]. Both patients fully recovered within 1 to 2 months after discontinuation of treatment. One patient experienced a recurrence of liver injury (ALT 3226 U/L, ALP 140 U/L, bilirubin 10.9 mg/dL) within 28 days of restarting treatment, which was more severe than the initial episode, but resolved spontaneously within 2 months of discontinuation of treatment. In both cases, the possibility of other diagnoses remains.
Probability Score: D (Possibly a rare cause of clinically significant liver damage).

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Effects during Pregnancy and Lactation
◉ Overview of Use During Lactation
There is currently no information regarding the clinical use of retemertil during lactation. Because retemertil binds to plasma proteins at a rate exceeding 99%, its levels in breast milk are likely to be low. If a mother needs to take retemertil, she should not discontinue breastfeeding. Until more data are available, breastfeeding women using retemertil should closely monitor their infants, especially newborns or premature infants.
◉ Effects on Breastfed Infants
No relevant published information was found as of the revision date.
◉ Effects on Lactation and Breast Milk
No relevant published information was found as of the revision date.

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- In acute toxicity studies, no deaths were observed in mice at doses up to 200 mg/kg. [1] - In rats, long-term administration (10 mg/kg/day for 28 days) did not cause significant changes in liver and kidney function indicators. [1] - In preclinical models, no adverse effects on bone mineral density or cardiac structure were detected. [1] - In clinical trials, common adverse events included transient diarrhea (33%) and nausea (14%), ranging from mild to moderate. [7]

[1]. Discovery of 2-[3,5-dichloro-4-(5-isopropyl-6-oxo-1,6-dihydropyridazin-3-yloxy)phenyl]-3,5-dioxo-2,3,4,5-tetrahydro[1,2,4]triazine-6-carbonitrile (MGL-3196), a Highly Selective Thyroid Hormone Receptor β agonist in clinical trials for the treatment of dyslipidemia. J Med Chem. 2014 May 22;57(10):3912-23.
[2]. Activation of thyroid hormone receptor-β improved disease activity and metabolism independent of body weight in a mouse model of non-alcoholic steatohepatitis and fibrosis. Br J Pharmacol. 2021 Jun;178(12):2412-2423.
[3]. A new mechanism of thyroid hormone receptor β agonists ameliorating nonalcoholic steatohepatitis by inhibiting intestinal lipid absorption via remodeling bile acid profiles. Acta Pharmacologica Sinica. 2024 Oct;45(10):2134-2148.

MGL-3196 has been used in trials investigating its treatment for non-alcoholic steatohepatitis (NASH) and heterozygous familial hypercholesterolemia. Resmetirom is a thyroid hormone receptor beta (THR-β) agonist used in combination with diet and exercise to treat moderate to severe fibrotic NASH. Mild and transient elevations in serum transaminases may occur during the first month of Resmetirom treatment, and in rare cases, acute liver injury may occur, which can be severe but is reversible upon discontinuation of the drug.

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Drug Indications
Treatment of Non-Alcoholic Steatohepatitis (NASH) Resmetirom is a thyroid hormone receptor beta (THR-β) agonist. On March 14, 2024, the U.S. Food and Drug Administration (FDA) approved Resmetirom as the first drug for the treatment of liver fibrosis caused by non-alcoholic steatohepatitis (NASH). NASH is a type of non-alcoholic fatty liver disease (NAFLD). Thyroid hormones directly regulate lipid metabolism in the liver; therefore, NAFLD patients often exhibit impaired thyroid function, such as decreased serum thyroid hormone levels. Resmetirom reduces liver fat by stimulating fatty acid degradation and oxidation. Resmetirom is a thyroid hormone receptor β agonist. Its mechanisms of action include acting as a thyroid hormone receptor β agonist, a cytochrome P450 2C8 inhibitor, an organic anion transport peptide 1B1 inhibitor, an organic anion transport peptide 1B3 inhibitor, and a breast cancer resistance protein inhibitor. Resmetirom is a small molecule drug that has completed the most Phase IV clinical trials (covering all indications) and was first approved in 2024 for the treatment of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, with three investigational indications.
Thyroid Hormone Receptor Beta Agonist
Drug Indications
Resmetirom is indicated for use in combination with diet and exercise to treat adult patients with noncirrhotic nonalcoholic steatohepatitis (NASH) with moderate to severe liver fibrosis (consistent with F2 to F3 stage fibrosis). It should be avoided in patients with decompensated cirrhosis. This indication received accelerated approval based on improvement in NASH and fibrosis. Continued approval for this indication may be contingent upon validation and description of clinical benefit in confirmatory trials.
Pharmacodynamics
Resmetirom is a partial agonist of thyroid hormone receptor beta (THR-β). In in vitro THR-β activation function trials, Resmetirom achieved 83.8% efficacy against triiodothyronine (T3) with an EC50 of 0.21 µM. In the same thyroid hormone receptor α (THR-α) agonist function test, resmetirom showed a efficacy of 48.6% relative to T3, with an EC50 of 3.74 µM. Resmetirom reduces hepatic fat content and the concentration of free thyroxine (FT4), a prothyroid hormone. Although inconclusive, there are reports in the literature suggesting that resmetirom may convert thyroxine (T4) to triiodothyronine (T3). It also increases the concentration of sex hormone-binding globulin. Mechanism of Action: Thyroid hormones, such as free thyroxine (FT4) and free triiodothyronine (FT3), are key regulators of hepatic lipid metabolism. Thyroid hormone receptor β (THR-β) is the main thyroid hormone receptor in the liver; stimulation of this receptor reduces intrahepatic triglyceride levels. Many patients with non-alcoholic fatty liver disease (NAFLD) have thyroid dysfunction, such as hypothyroidism, making it a significant risk factor for NAFLD. Hypothyroidism is also associated with lipolysis of adipose tissue and increased release of free fatty acids from adipose tissue to the liver, thereby promoting hepatic insulin resistance. Elevated levels of circulating pro-inflammatory adipokines, which can lead to liver inflammation and fibrosis, have also been observed. Resmetirom is a partial agonist of THR-β that promotes lipophagy and hepatic fatty acid β-oxidation, thereby reducing hepatic fat. It is about 28 times more selective for THR-β than for FT3, but less selective for thyroid hormone receptor α (THR-α), which is mainly expressed in the heart and bones. Resmetirom (MGL-3196) is a liver-targeting THR-β agonist designed to avoid the effects of THR-α on the heart and bones. [1] Its mechanism of action includes promoting fatty acid oxidation, reducing de novo lipogenesis and regulating bile acid metabolism, thereby improving the pathology of non-alcoholic steatohepatitis (NASH). [2,3]- This drug received accelerated approval from the FDA in 2024 for the treatment of moderate to severe fibrotic (F2-F3) nonalcoholic steatohepatitis (NASH). [1,7]- In a phase 3 clinical trial, 25.9% to 29.9% of patients achieved remission of NASH after 52 weeks of treatment, with no worsening of fibrosis. [7]

C17H12CL2N6O4

435.22

434.03

C, 46.92; H, 2.78; Cl, 16.29; N, 19.31; O, 14.70

920509-32-6

15981237

Typically exists as Yellow to orange solids at room temperature

1.65±0.1 g/cm3 (20 °C, 760 mmHg)

2.098

2

7

4

29

878

0

N#CC1C(=O)NC(=O)N(C2C=C(Cl)C(OC3C=C(C(C)C)C(=O)NN=3)=C(Cl)C=2)N=1

FDBYIYFVSAHJLY-UHFFFAOYSA-N

InChI=1S/C17H12Cl2N6O4/c1-7(2)9-5-13(22-23-15(9)26)29-14-10(18)3-8(4-11(14)19)25-17(28)21-16(27)12(6-20)24-25/h3-5,7H,1-2H3,(H,23,26)(H,21,27,28)

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: ≥ 3.75 mg/mL (8.62 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 37.5 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 2: ≥ 3.75 mg/mL (8.62 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 37.5 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 3: ≥ 3.75 mg/mL (8.62 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 37.5 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.)