Octinoxate acts as a thyroid hormone disruptor by targeting thyroid hormone receptors (TRα and TRβ), inhibiting thyroid hormone (T3/T4)-mediated transcriptional activity[1]

In HEK293T cells transfected with TRα/TRβ and thyroid hormone-responsive luciferase reporter plasmid, Octinoxate (1-100 μM) dose-dependently inhibited T3-induced luciferase activity: 50 μM reduced TRα-mediated activity by ~45% and TRβ-mediated activity by ~50% vs. T3-only group[1]
In rat thyroid follicular epithelial cells (FRTL-5), Octinoxate (5-50 μM) downregulated mRNA levels of thyroid-specific genes: 25 μM decreased thyroid peroxidase (TPO) by ~35%, thyroglobulin (Tg) by ~40%, and sodium-iodide symporter (NIS) by ~30% (real-time RT-PCR)[1]
Octinoxate (up to 100 μM) showed no significant cytotoxicity in FRTL-5 cells (MTT assay, cell viability > 85% vs. control)[1]
In primary human thyroid cells, Octinoxate (20 μM) reduced T4 secretion by ~25% after 48 h treatment (ELISA detection)[1]

In zebrafish embryos exposed to Octinoxate (0.1-1 μM) from 4 h post-fertilization (hpf) to 96 hpf: 0.5 μM increased embryo mortality by ~15%, induced developmental abnormalities (e.g., curved spine, pericardial edema) in ~20% of embryos, and reduced whole-body T3 levels by ~30% (LC-MS/MS detection)[1]
In adult zebrafish exposed to Octinoxate (0.2 μM) for 28 days: thyroid follicles showed reduced size (~25% smaller) and increased colloid depletion (~30% vs. control), and hepatic mRNA levels of TRβ were upregulated by ~40% (real-time RT-PCR)[1]
In Sprague-Dawley rats orally administered Octinoxate (10/50 mg/kg/day) for 28 days: 50 mg/kg group showed serum T4 levels decreased by ~20%, serum TSH levels increased by ~15% (ELISA), and thyroid gland weight increased by ~10% vs. vehicle control[1]

Thyroid peroxidase (TPO) activity assay: Recombinant human TPO (50 ng) was mixed with Octinoxate (1-50 μM) in reaction buffer (50 mM phosphate buffer pH 7.4, 0.1 mM KI, 0.01 mM H2O2). L-tyrosine (0.1 mM) was added as substrate, and the mixture was incubated at 37°C for 60 min. The amount of iodinated tyrosine (product) was measured by HPLC at 280 nm, and TPO inhibition rate was calculated[1]
TR-mediated transcriptional activity assay: HEK293T cells were seeded in 24-well plates, transfected with pCMV-TRα/pCMV-TRβ, pGL3-TRE-luciferase, and pRL-TK-Renilla (internal control). After 24 h, cells were treated with Octinoxate (1-100 μM) + T3 (10 nM) for 16 h. Luciferase activity was detected by dual-luciferase kit, normalized to Renilla[1]

FRTL-5 cell gene expression assay: FRTL-5 cells were cultured in Ham’s F-12 medium with thyroid-stimulating hormone (TSH, 1 mU/mL). Cells were treated with Octinoxate (5-50 μM) for 48 h. Total RNA was extracted, cDNA synthesized, and real-time RT-PCR performed with primers for TPO, Tg, NIS, and GAPDH (internal control). Relative gene expression was calculated by 2^(-ΔΔCt) method[1]
Primary human thyroid cell T4 secretion assay: Primary human thyroid cells were isolated from normal thyroid tissue, cultured in DMEM/F12 medium. Cells were treated with Octinoxate (5-40 μM) for 48 h. Culture supernatants were collected, and T4 levels were quantified by sandwich ELISA (detection wavelength 450 nm)[1]
FRTL-5 cell viability assay: Cells were seeded in 96-well plates (5×10³ cells/well), treated with Octinoxate (1-100 μM) for 72 h. MTT solution (0.5 mg/mL) was added for 4 h, DMSO dissolved formazan, and absorbance at 570 nm was measured to calculate viability[1]

Zebrafish embryo exposure model: Wild-type zebrafish embryos were collected within 4 hpf, placed in 6-well plates (30 embryos/well) containing Octinoxate solution (0.1/0.5/1 μM, prepared in E3 medium). Embryos were incubated at 28°C under 14 h light/10 h dark cycle. Mortality and developmental abnormalities were recorded at 24/48/72/96 hpf; at 96 hpf, embryos were homogenized for T3 level detection (LC-MS/MS)[1]
Adult zebrafish exposure model: Adult zebrafish (6 months old, 1:1 male:female) were placed in aquaria containing Octinoxate solution (0.2 μM, refreshed every 48 h) for 28 days. At the end of exposure, zebrafish were euthanized; thyroid glands were fixed for histology (HE staining, follicle size measurement), and livers were collected for real-time RT-PCR (TRβ gene detection)[1]
Rat oral administration model: Male Sprague-Dawley rats (8 weeks old) were randomized into 3 groups: vehicle (corn oil, 10 mL/kg), Octinoxate 10 mg/kg, Octinoxate 50 mg/kg. Drugs were administered by oral gavage once daily for 28 days. On day 29, rats were euthanized; blood was collected for serum T4/TSH detection (ELISA), and thyroid glands were weighed and fixed for histology[1]

Absorption, Distribution and Excretion
After skin application, it can be absorbed systemically and is present in the deep stratum corneum, as well as in urine, plasma, and breast milk. The mean maximum plasma concentration detected after applying 2 mg/cm² sunscreen was 7 ng/mL in women and 16 ng/mL in men. It can be detected unchanged in urine. Nude mouse skin. The study was conducted in a laboratory chamber. Most of the substance was present in the shed skin; less was found in the stratum corneum, and the least was found in the laboratory chamber. The substance concentrations detected in the laboratory chamber were approximately: 1.13% after 6 hours; 11.4% after 16 hours; and 17.9% after 24 hours. The total dose percentages of the stratum corneum and shed skin were 31.4%, 44.4%, and 45.7%, respectively. Similar results were obtained with 3% and 20% AI solutions. Small amounts of radioactive AI were applied to the interscapular region of eight healthy volunteers. One group of four volunteers applied AI under a petri dish; the other four volunteers applied AI to gauze, one of whom underwent occlusion. Except for approximately 0.2% AI detected in urine, all other AI absorption tests were negative. The concentrations used were not specified. In a preliminary experiment, subjects orally ingested a capsule containing 100 mg AI. …The cumulative excretion of 4-methoxycinnamic acid ester in urine over 24 hours was investigated using gas chromatography-mass spectrometry (GC/MS) to detect the methyl ester derivative. (This method can also detect 4-hydroxycinnamic acid). 13.2% of the ingested amount was recovered within 24 hours, equivalent to 21.5% of the expected amount of the active ingredient to be completely absorbed. The main part of the experiment used a water-in-oil cream containing 10% of the active ingredient. 2 grams of this cream (= 200 mg of active ingredient) was applied to the interscapular region of five male subjects aged 29 to 46 years. The application area was 25 × 30 cm. After application, the area was covered with three layers of gauze and left for 12 hours. Blood samples were collected at 0, 0.5, 1, 2, 3, 5, 7, and 24 hours. Urine samples were collected at 0, 1, 2, 3, 4, 5, 6, 7, 12, 24, 48, 72, and 96 hours. Control plasma samples had a concentration of approximately 10 ng/ml before administration. No increase in plasma concentration was observed during the experiment. Urine sample concentrations were within the “physiological” range, from 100 to 300 ng/ml. No significant increase in this concentration was observed in any samples. The authors concluded that the compound was barely absorbed under the experimental conditions. This study aimed to determine the effect of a carrier on the penetration of octyl methoxycinnamate (OMC) as a UV absorber into the stratum corneum using a stripping method. Experimental formulations included conventional water-in-oil emulsions and multilayer liposomes (MLVs) and small monolayer liposomes (SUVs) containing OMC. MLVs containing OMC were prepared by a melt method and then converted to SUVs by probe sonication. Subsequently, different formulations were applied to the palmar side of the forearm of six volunteers at a dose of 2 mg/cm². After predetermined time points, a peel-off method was used, involving the application of 22 strips of adhesive tape, and subjects were divided into different peel-off groups. High-performance liquid chromatography (HPLC) was used to evaluate the sunscreen agents, and the sun protection factor (SPF) of the formulations was determined in human volunteers according to Australian standards. Overall results showed that multilayer liposomes (MLVs) exhibited significantly higher skin accumulation of OMC compared to water-in-oil emulsions and single-layer vesicles (SUVs). Furthermore, SUVs penetrated significantly deeper into the skin layers than MLVs and conventional water-in-oil emulsions. Simultaneously, in all tested formulations, the amount of OMC recovered from the upper stratum corneum was higher than that from the deeper layers. Finally, the SPF value of liposomes containing OMC was slightly higher than that of the control emulsion with the same concentration of OMC. In summary, the results of this study indicate that multilayer liposomes (MLVs) prepared by the melt method may be a superior sunscreen carrier for octyl oxytocin (OMC) because they offer a slightly higher SPF compared to conventional formulations and retain more drug in the stratum corneum, thus reducing its penetration into deeper layers. For more complete data on the absorption, distribution, and excretion of octyl oxytocin (19 in total), please visit the HSDB record page. Metabolites/Metabolites: Systemically absorbed, it is metabolized in the liver. It can be degraded by lipases in the stratum corneum, where esters are hydrolyzed. Exposure to sunlight degrades it into photoproducts, leading to reduced UV absorption efficiency. As a lipophilic substance, this active ingredient is likely to be metabolized; it is known to be hydrolyzed by plasma esterases, although at a slow rate.

Protein Binding
No Interaction This encourages agricultural workers to use sunscreen to reduce the risk of UV-related skin cancer. Previous studies have shown that some commercially available sunscreens have penetration-enhancing effects. This project aims to determine whether the active ingredients in sunscreen formulations (i.e., the UV-absorbing components and insect repellents in sunscreen/insect repellent combinations) can also act as skin penetration enhancers for herbicides in vitro. Within 24 hours, the total percentage of 2,4-dichlorophenoxyacetic acid (2,4-D) penetrating the skin of hairless mice ranged from 54.9 ± 4.7% in the control group that had never applied sunscreen to 86.9 ± 2.5% in the pardimat-O group. Of the active ingredients tested (7.5% octyl methoxycinnamate, 7% octocrylene, 0.6% oxybenzone, 5% homosalate, 5% octyl salicylate, 8% pardimethicone-O, 10% sulfonylurea benzophenone, and 9.5% and 19% N,N-diethyl-m-toluamide (DEET)), all except octocrylene significantly increased the total permeability of 2,4-D (P < 0.05 compared to the control group), and only octocrylene and oxybenzone did not significantly shorten the corresponding hysteresis time. Octyl salicylate (P < 0.01) and octyl methoxycinnamate (P < 0.05) significantly increased the trihydrate permeability of 2,4-D in mouse skin, indicating that they caused physical damage to the stratum corneum. Further studies showed that the enhanced permeation observed in hairless mouse skin also existed in human skin. Therefore, the active ingredients in sunscreen formulations can enhance the skin penetration of the moderately lipophilic herbicide 2,4-D. The authors aimed to determine whether pre-application of a sunscreen with SPF 29 (containing octyl methoxycinnamate, oxybenzone, and octyl salicylate) could prevent the inhibition of contact hypersensitivity reactions to dinitrochlorobenzene (DNCB) induced by localized UVB irradiation. Nineteen subjects received two types of irradiation in a 16 cm² area of the buttocks: a UVB group receiving the minimum erythema dose of UVB three times daily for three consecutive days; and a UVB group receiving the same dose of UVB irradiation after applying sunscreen. One day after the irradiation ended, DNCB was applied to the buttocks; two weeks later, a DNCB challenge test was performed on the forearms using four different concentrations of DNCB. A control group of 10 subjects received the same DNCB test but had no prior UVB exposure (no UVB group). ...Compared to the UVB-free control group, the UVB group showed decreased response rates to all DNCB stimulation doses (3.125, 6.25, and 8.8 μg), except for the highest dose (12.5 μg) (Fisher's exact test, P ≤ 0.008); the UVB group also showed decreased response rates compared to the sunscreen plus UVB group (P ≤ 0.02). There were no significant differences in response rates to all tested doses of DNCB between the UVB-free group and the sunscreen plus UVB group (P ≥ 0.53). …These results indicate that using sunscreen with a protective power nine times higher than that required to prevent erythema before local UVB exposure can prevent and inhibit local UVB-induced contact hypersensitivity reactions…
This study evaluated the effects of sucrose laurate and sucrose oleate on the in vivo percutaneous penetration of octyl methoxycinnamate (OMC) formulations, including i) colloidal suspensions (nanoemulsions and nanocapsules) and ii) conventional water-in-oil (o/w) emulsions. Results showed that nanoemulsions with added sucrose laurate exhibited the highest permeability in the stratum corneum compared to other formulations. Compared to the control group, nanoemulsions with added sucrose laurate doubled the amount of OMC deposited in the skin. The data obtained indicate that the total amount of OMC detected in the stratum corneum and its penetration depth are closely related to the nature of the formulation, particle size, and type of synergist.
Hairless mice were exposed to repeated ultraviolet radiation irradiation simulating the solar spectrum. After a rest period, 12-O-tetradecanoylphorbol-13-acetate was applied to the skin of mice three times a week… and a suitable control group was set up. The experimental group was completely protected at a 50% concentration, while the effect at a 7.5% concentration was equivalent to a four-fold reduction in sunlight intensity. It has been suggested that artificial intelligence itself may act as a promoter, but there is no evidence to support this view. For more complete data on interactions of octyl methoxycinnamate (7 in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats >20 mL/kg body weight
Oral LD50 in mice >8 g/kg body weight
In zebrafish embryos, octyl methoxycinnamate (1 μM) caused approximately 25% mortality and approximately 30% developmental abnormalities after 96 hours; no significant acute toxicity was observed at a concentration of 0.1 μM [1]
In rats, continuous administration of octyl methoxycinnamate (50 mg/kg/day) for 28 days induced thyroid hyperplasia (an increase in the number of follicles of approximately 15%), but no significant damage was observed (serum AST/ALT and creatinine levels were unchanged compared with the control group) [1]

[1]. Octinoxate as a potential thyroid hormone disruptor - A combination of in vivo and in vitro data. Sci Total Environ. 2023 Jan 15;856(Pt 1):159074.

2-Ethylhexyl methoxycinnamate is a colorless to pale yellow viscous liquid. (NTP, 1992)
Octyl 4-methoxycinnamate is a cinnamic acid ester.
Octyl methoxycinnamate is a cinnamic acid ester and a common ingredient in sunscreens and other skincare products used to reduce DNA photodamage. Originally developed in the 1950s, it is an organic UV-B filter that absorbs UV-B rays from sunlight. It is often used in combination with nanoparticles or other waterproof liposomes to increase its localization on the epidermis and reduce the risk of transdermal absorption. Its use in pharmaceutical and cosmetic formulations has been approved by the FDA.
See also: Avobenzone; Octyl methoxycinnamate; Oxybenzone (ingredient); Octyl methoxycinnamate; Octocrylene (ingredient); Arbutin; Octyl methoxycinnamate (ingredient)...See more...
Pharmaceutical Indications
As an active ingredient in sunscreens and lip balms. Used to protect skin from the harmful effects of sunlight.

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Mechanism of Action
Octyl methoxycinnamate primarily absorbs UV-B and UV-A rays and accumulates in the outermost layer of the epidermis. Like other photoprotectants, octyl methoxycinnamate prevents cell and DNA damage by reducing p53 protein expression after UV exposure and improves skin tolerance to UV radiation.
By absorbing UV radiation within a specific wavelength range, it reduces UV penetration into the epidermis. The molecular structure of sunscreens affects the amount and wavelength of UV absorption. /Sunscreen, Topical/
The principle of radiation absorption by chemical sunscreens is that the electronic energy levels of the drug transition from the ground state to higher energy levels or excited states. Chromophores with loose electrons (C=C, C=O, ON=O) are easily excited by radiation. Compounds with multiple chromophores in optimal positions have higher absorption rates over a wider wavelength range. Chemical sunscreens typically absorb at least 85% of UVB radiation (thus preventing sunburn) but may allow UVA radiation to pass through (thus allowing tanning). Some sunscreens may have a slightly wider or narrower absorption range than UVB. All para-aminobenzoic acid (PABA) derivatives absorb light with wavelengths around 290-320 nm, benzophenone derivatives around 250-360 nm, cinnamic acid derivatives around 280-320 nm, and salicylate derivatives and some other chemical sunscreens around 270-320 nm. For many years, it was believed that the wavelength at which the skin is most sensitive was 296.7 nm; however, recent evidence suggests that the UVB wavelengths most likely to cause erythema may be slightly lower (e.g., in the 292-295 nm range). Furthermore, most of the stronger burning wavelengths reaching the Earth's surface are around 310 nm. Therefore, sunscreens that can absorb UVB radiation at its maximum absorption rate near these two wavelengths are particularly effective in preventing sunburn. The maximum absorption wavelength of para-aminobenzoic acid (PABA) is around 290 nm, that of glyceryl para-aminobenzoate is around 295 nm, and that of the remaining PABA derivatives is around 310 nm. The maximum absorption wavelength of benzophenone derivatives is 280-290 nm, that of cinnamic acid derivatives is 310 nm (but the maximum absorption wavelength of diethanolamine methoxycinnamate is 290 nm), and that of salicylic acid derivatives and some other sunscreens is 300-305 nm. /Sunscreen/

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Therapeutic Use
UV/UVB/Protection
/Author/Based on the FDA Sunscreen Monograph, the sun protection factor (SPF) of a hydroquinone formulation (Lustra-Ultra, Taro Pharma, Hawthorne, NY) containing 3% avobenzone and 7.5% octyl methoxycinnamate was tested on 20 volunteers. We also determined the UV absorption spectrum of this formulation. …The average SPF was 21.7, meeting the SPF 20 labeling requirement. This formulation exhibited the strongest photoprotective effect near the sunburn peak wavelength in the UVB region and maintained significant UV absorption throughout the UVA region. 3% avobenzone and 7.5% octyl methoxycinnamate provide broad-spectrum UV protection. Adding these sunscreens to hydroquinone formulations simplifies treatment regimens and provides significant photoprotection for patients undergoing treatment for pigmentation disorders. Sunscreens that inhibit erythema are thought to also prevent UV-induced carcinogenesis. However, the correlation between inflammation and carcinogenesis remains unclear, and prevention of UV-induced erythema may actually be biologically unrelated to prevention of UV-induced skin cancer. UVB radiation promotes skin immunosuppression by releasing immunomodulatory cytokines and depleting Langerhans cells. This study investigated the ability of two different sunscreens to inhibit UVB-induced epidermal interleukin (IL)-10 expression and Langerhans cell depletion. Chemical and physical sunscreens were applied to the forearms of volunteers 15 minutes before irradiation with four minimum erythema doses of UVB. Blisters were induced 24 hours after irradiation, and RNA was extracted from the tops of the blisters. Reverse transcription polymerase chain reaction (RT-PCR) was performed using IL-10 and CD1a primers. Two sunscreens were tested: a chemical sunscreen containing octyl methoxycinnamate (SPF 12) and a physical sunscreen containing zinc oxide (SPF 16). Both sunscreens almost completely inhibited UVB-induced IL-10 mRNA expression (median protection rates of 95% and 78% for the chemical and physical sunscreens, respectively), while partially inhibiting UVB-induced Langerhans cell exhaustion (inhibition rates of 47% and 50% for the chemical and physical sunscreens, respectively). Cell density estimation after ATPase staining confirmed the protective effect of the sunscreens on Langerhans cells. Conversely, both sunscreens effectively prevented UVB-induced erythema. The authors consider this the first demonstration that sunscreen can prevent the induction of skin immunosuppressive mediators, and the results indicate that the immunoprotective effect provided by sunscreen is far lower than its ability to prevent erythema. It is recommended that residents living in areas with high solar radiation, those working outdoors, or those who frequently engage in outdoor recreational activities use a sunscreen with an SPF higher than 15 daily on normally exposed skin. Daily use of sunscreen can reduce the cumulative sun exposure that can lead to actinic keratosis and squamous cell carcinoma. Sunscreen is intended to prevent sunburn. In addition to limiting the time skin is exposed to sunlight, regular use of sunscreen in the sun can help reduce long-term sun damage, such as premature skin aging and skin cancer. US product labels include a /

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Drug Warning
Manufacturers of sunscreens using propellants warn that inhaling the fumes produced by these formulations can be harmful or even fatal. /Propellant/
Because the skin absorption characteristics of infants under 6 months of age may differ from those of adults, and their metabolic and excretory pathways are not yet mature, potentially limiting their ability to clear transdermal sunscreens, sunscreen products should only be used on infants under the guidance of a clinician. The skin characteristics of older adults may also differ from those of younger adults, but these characteristics and the special considerations for using sunscreen in this age group are not fully understood. /Sunscreen/
Information on the safety of long-term use of sunscreen is scarce, but commercially available physical and chemical sunscreens appear to have a low incidence of adverse reactions. Derivatives of para-aminobenzoic acid (PABA), benzophenone, cinnamic acid, salicylates, and 2-phenylbenzimidazole-5-sulfonic acid can cause skin irritation in rare cases, including burning, stinging, itching, and erythema. /Sunscreen/
Sunscreen should not be used to extend the duration of sun exposure, such as prolonged sunbathing, nor should it be applied to clothing on areas not normally exposed to sunlight, such as the torso and buttocks. /Sunscreen/
For more complete data on drug warnings for octinoxate (11 in total), please visit the HSDB record page.

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Pharmacodynamics
As a photoprotectant, it protects the skin by preventing and minimizing the harmful effects of ultraviolet (UV) radiation from natural light. Cellular effects of UV radiation include DNA damage, cell cycle arrest, immunosuppression, apoptosis, and transcriptional alterations. Octyl methoxycinnamate (2-ethylhexyl-4-methoxycinnamate) is a widely used ultraviolet B (UVB) filter that is often added to sunscreens and cosmetics [1]. Octyl methoxycinnamate interferes with thyroid function through two pathways: 1) competing with T3 for the binding site of TRα/TRβ, inhibiting TR-mediated transcriptional activation; 2) downregulating the expression of thyroid-specific genes (TPO, Tg, NIS), thereby reducing the synthesis and secretion of thyroid hormones [1]. Octyl methoxycinnamate can enter aquatic environments (e.g., rivers, oceans) through wastewater discharge, posing a potential risk to aquatic organisms (e.g., zebrafish) by interfering with thyroid function [1].

C18H26O3

290.39724

290.188

5466-77-3

5355130

Light yellow to yellow liquid

1.0±0.1 g/cm3

405.3±20.0 °C at 760 mmHg

less than -13 °F (NTP, 1992)
-25°C
-68.3 °C using OECD Guideline 102 (Melting point/Melting Range)

171.6±16.4 °C

0.0±0.9 mmHg at 25°C

1.515

5.66

0

3

10

21

304

0

O=C(OCC(CC)CCCC)/C=C/C1=CC=C(OC)C=C1

YBGZDTIWKVFICR-JLHYYAGUSA-N

InChI=1S/C18H26O3/c1-4-6-7-15(5-2)14-21-18(19)13-10-16-8-11-17(20-3)12-9-16/h8-13,15H,4-7,14H2,1-3H3/b13-10+

2-ethylhexyl (E)-3-(4-methoxyphenyl)prop-2-enoate

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)

Ethanol : ~140 mg/mL (~482.09 mM)
DMSO : ~1 mg/mL (~3.44 mM)
H2O : ~0.67 mg/mL (~2.31 mM)

Solubility in Formulation 1: 3.5 mg/mL (12.05 mM) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 35.0 mg/mL clear EtOH 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: 3.5 mg/mL (12.05 mM) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 35.0 mg/mL clear EtOH 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: ≥ 3.5 mg/mL (12.05 mM) (saturation unknown) in 10% EtOH + 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 35.0 mg/mL clear EtOH stock solution to 900 μL of corn oil and mix well.

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