Absorption, Distribution and Excretion
Systemic exposure to hydroquinone was assessed in eight healthy subjects after two weeks of twice-daily topical application of a hydroquinone-retinoic acid combination. A dose equivalent to approximately 37.3 μg/cm² of hydroquinone was applied to the back of the subjects. The mean Cmax of hydroquinone was 9.92 ng/mL (range 4.22 to 23.62 ng/mL), and the Tmax was 2 hours (range 1 to 2 hours). The safety of hydroquinone in this combination formulation has been demonstrated by the low systemic exposure in the subjects. Hydroquinone is primarily excreted via the kidneys as a metabolite. The volume of distribution indicates that hydroquinone is distributed throughout the body water, and intracellular concentrations are expected to be similar to rough measurements. Currently, readily available data on hydroquinone clearance are unavailable. Hydroquinone-containing products are typically used for topical application. Solage is a compound preparation consisting of 2% hydroquinone (4-hydroxyanisole) and 0.01% retinoic acid (all-trans retinoic acid) dissolved in ethanol… This study aimed to assess the transdermal absorption of [(3)H]retinoic acid and estimate the systemic exposure to hydroquinone after topical application of this compound preparation to the back of healthy subjects. Eight subjects had a non-radiolabeled 2% menadione/0.01% retinoic acid solution applied topically twice daily to a 400 cm² area on their backs for 14 days. Afterward, subjects received a single topical application of 2% menadione/0.01% (³H)retinoic acid solution. Twelve hours later, the radiolabeled drug was removed, and the non-radiolabeled 2% menadione/0.01% retinoic acid solution was applied topically twice daily for 7 days. Total radioactivity in plasma, urine, and fecal samples was analyzed using gas chromatography-mass spectrometry (GC/MS), and the levels of menadione and retinoic acid in plasma were also analyzed. Based on the cumulative radioactive recovery rates in urine and feces, the mean dermal absorption rate of [³H]retinoic acid was approximately 4.5% (median 2.18%). Plasma retinoic acid concentrations did not exceed endogenous levels. This is consistent with plasma radioactive material concentrations, with a mean Cmax of 91 pg-eq/mL (median 26 ng/mL). The mean Cmax and AUC (0–12 hr) values for hydroquinone were 10 ng/mL and 33 ng·h/mL, respectively. Based on these results, topical application of retinoic acid in this formulation is unlikely to cause systemic toxicity, as retinoic acid absorption through the skin is minimal, and endogenous retinoic acid levels did not increase after twice-daily administration of this compound formulation. The systemic exposure in this study was significantly lower than the highest-dose systemic exposure in mouse (16.6 times) and rat (34.6 times) dermal toxicity studies, supporting the safety of hydroquinone in this compound formulation. In a study of healthy subjects, participants applied 0.8 mL of a compound preparation containing 2% hydroquinone and 0.01% retinoic acid twice daily to a 400 cm² area of their back skin for 14 days. Results showed that approximately 4.5% of the radiolabeled dose was recovered in urine and feces as retinoic acid. Plasma retinoic acid concentrations in this study did not exceed endogenous plasma concentrations, and the mean peak plasma hydroquinone concentration was approximately 10 ng/mL. /Solage/
There are also indications that…the substance can be absorbed to toxic doses in solution, especially at sites of skin breakage.

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Metabolism/Metabolites
Analysis of urine samples from melanoma patients treated with hydroquinone identified several hydroquinone metabolites, including 3,4-dihydroxyanisole, two o-methyl derivatives, 3-hydroxy-4-methoxyanisole and 4-hydroxy-3-methoxyanisole, and even hydroquinone, which may be at least partially derived from hydroquinone. All of these identified metabolites are primarily excreted as sulfates and glucuronides—only small amounts are present in urine in unbound forms. Ultimately, 3,4-dihydroxyanisole is considered the most important metabolite of hydroquinone. One treatment for malignant melanoma targeting tyrosinase involves the use of depigmented phenolic prodrugs, such as 4-hydroxyanisole (4-HA), which are oxidized by melanoma tyrosinase to produce cytotoxic orthoquinones. However, in a recent clinical trial, both renal and hepatic toxicity were reported as side effects of 4-HA treatment. In the following experiment, intraperitoneal injection of 4-HA (200 mg/kg) in mice resulted in a 7-fold increase in plasma transaminase levels, indicating hepatotoxicity. Furthermore, 4-HA-induced cytotoxicity in isolated hepatocytes was preceded by glutathione (GSH) depletion, which was prevented by cytochrome P450 inhibitors, partially inhibiting the cytotoxicity. The 4-HA metabolite generated from NADPH/microsomes and GSH was identified as a hydroquinone monoglutathione conjugate. GSH-depleted hepatocytes are more susceptible to 4-HA or its active metabolite hydroquinone (HQ)-induced cytotoxicity. Dicoumarol (an inhibitor of NAD(P)H/quinone oxidoreductase) also enhanced 4-HA or HQ-induced toxicity, while sorbitol (an NADH-generating nutrient) inhibited this cytotoxicity. Ethylenediamine (an ortho-quinone scavenger) failed to inhibit 4-HA-induced cytotoxicity, suggesting that this cytotoxicity is not caused by ortho-quinones generated from the cyclohydroxylation of 4-HA. Neither deferoxamine nor the antioxidant pyrogallol/4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxy (TEMPOL) prevented 4-HA-induced cytotoxicity, thus ruling out oxidative stress as a possible mechanism of 4-HA cytotoxicity. The amount of formaldehyde generated when 4-HA was incubated with rat microsomes/NADPH was negligible. These results indicate that the cytotoxic mechanism of 4-HA involves 4-HA epoxides or alkylation of quinones onto cellular proteins, rather than oxidative stress. Many common depigmenting agents, such as hydroquinone and 4-hydroxyanisole, are actually melanocyte-toxic chemicals that oxidize in melanocytes to produce highly toxic compounds, such as quinones. These cytotoxic compounds damage pigment cells, leading to skin depigmentation. However, cells can protect themselves from cytotoxic substances through intracellular glutathione (GSH). This protection is achieved through the enzymatic action of the detoxification enzyme glutathione S-transferase (GST), which is responsible for binding toxic substances to GSH. Studies have shown that sulfoxide (BSO) and cystamine can reduce intracellular GSH levels, thereby enhancing the depigmenting effect of hydroquinone. Furthermore, BSO and cystamine can also inhibit GST activity. All-trans retinoic acid (TRA) also exhibits a synergistic depigmenting effect when used in combination with hydroquinone or 4-hydroxyanisole. TRA is a potent mammalian GST inhibitor that makes cells more susceptible to the cytotoxic effects of chemicals by inhibiting GST activity. Studies have also shown that TRA can reduce intracellular GSH levels in certain cells. We propose that the mechanism by which TRA synergistically enhances the cytotoxic effects of chemicals on melanocytes involves inhibiting GST and attenuating glutathione-dependent cytoprotective effects, thereby counteracting melanocyte cytotoxicity.
1,4-Dimethoxybenzene is produced in guinea pigs, rats, rabbits, and mice. 4-Methoxycatechol, p-methoxyphenyl-β-D-glucuronide, and p-methoxyphenyl sulfate are produced in rabbits. /Excerpt from Table/
Known metabolites of 4-methoxyphenol include (2S,3S,4S,5R)-3,4,5-trihydroxy-6-(4-methoxyphenoxy)oxacyclohexane-2-carboxylic acid.

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Biological Half-Life
In melanoma patients, the elimination half-life of hydroquinone was 30 to 90 minutes 3 to 5 hours after intravenous infusion of 5 or 10 g/m²; similar values were reported after intra-arterial infusion.

Toxicity Summary
Identification and Uses: 4-Methoxyphenol (4-MP) is a colorless to white waxy solid or a white to brownish-red flaky crystalline substance with a caramel and phenolic odor. It is used as an inhibitor of acrylic acid monomers and acrylonitrile, a stabilizer for chlorinated hydrocarbons and ethyl cellulose, an ultraviolet inhibitor, and a chemical intermediate in the production of antioxidants, pharmaceuticals, plasticizers, and dyes. It is also used as a medicine to treat pigmentary abnormalities, especially hyperpigmentation, usually in combination with retinoic acid (Solage). Human Exposure and Toxicity: In 16 patients, 11 (69%; 95% confidence interval [CI], 41%–89%) achieved complete depigmentation after using 4-MP cream. Depigmentation symptoms usually appeared 4 to 12 months after application. Four patients (25%) reported mild burning or itching after using the cream. Of the 11 patients who responded to 4-MP cream, 4 experienced a relapse of pigmentation 2 to 36 months after discontinuation (relapse rate 36%; 95% CI, 11%–69%). Overuse of 4-MP can lead to significant redness, peeling, discomfort, or hypopigmentation. Oral administration of this drug may cause the same side effects as an overdose of oral vitamin A (vitamin A hyperacidity). In an ethylene dichloromethane plant, 2 out of 8 process workers exposed to hydroquinone monomethyl ether developed forearm depigmentation (occupational vitiligo), and one of them developed forehead depigmentation. A follow-up of two cases of vitiligo reported 8 years prior due to 4-MP exposure, and a survey of 169 men exposed to 4-MP or p-tert-amylphenol or both, revealed that one man experienced significant repigmentation and the other experienced mild repigmentation. Among 169 men surveyed at the same factory, screening using Wood's light technique (an ultraviolet light absorbed by normal pigmented skin and reflected by non-pigmented skin) revealed no cases of vitiligo associated with 4-MP exposure in either of the 148 men tested or the 129 men exposed to p-tert-amylphenol. Regarding potential genotoxicity, cytogenetic analysis indicated that a salt of 4-MP (p-methoxyphenol phosphate) reduced chromosome number and structural aberrations after the first passage of treated cells. Cytogenetic analysis also showed that the reduction in genetic instability in cell cultures treated with p-methoxyphenol phosphate in combination with benzo[a]pyrene appeared to remain constant between the first and sixth generations. Animal studies: Studies in rabbits showed that exposure to 4-MP could lead to severe necrosis if the exposure time exceeded one day. Prolonged exposure can cause severe burns. There are also indications that the substance can be absorbed to toxic doses in solution, especially in cases of broken skin. Acute parenteral poisoning in rabbits manifested as paralysis and hypoxia at low doses, and central nervous system depression at high doses. Topical application of 4-MP to guinea pigs (within 5 to 10 days post-treatment) and miniature pigs resulted in depigmentation of the skin. In rabbit skin teratogenicity studies, there were no statistically significant differences in fetal malformation data. However, significant hydrocephalus with prominent head bulging was observed in litters of pups in a moderate-dose group (4-MP and retinoic acid at 12 and 0.06 mg/kg or 132 and 0.66 mg/m², respectively). Topical application of 4-MP did not appear to be carcinogenic. In studies of twice-weekly application of 5% or 10% 4-MP (0.02 mL) to the interscapular region of mice (lasting 93 weeks) or the inner ear of rabbits, there was no significant reduction in survival or tumor incidence compared to the control group. Tumors were observed in F344 rats (30 males and 30 females) after 104 weeks of feeding with a diet containing 2% 4-MP. Histopathological findings in 4-MP cases included atypical hyperplasia (67% in males, 37% in females), papillomas (50%, 23%), and forestomach squamous cell carcinoma (77%, 20%). 4-MP induced forestomach papillomas (70%, 93%) and squamous cell carcinoma (53%, 37%), as well as submucosal hyperplasia of the proventriculus (90%, 93%), adenomas (100%, 100%), and adenocarcinoma (57%, 47%), accompanied by ulceration or erosion. No genotoxic effects were observed when 4-MP was tested in Salmonella Typhimurium TA98, TA100, TA1535, and TA1537, or in rats with 6 months of percutaneous exposure.

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Protein Binding
There is currently no readily available data on the protein binding of hydroquinone.Interaction
Tests were conducted in cultured Chinese hamster ovaries. This study used CHO cells (CHO-AA8-4 cell line) and X-ray irradiated Syrian hamster embryonic cells (SHE) to investigate the effects of butylated hydroxyanisole (BHA) on the metabolism and mutagenic activity of benzo[a]pyrene (BaP), comparing it with the effects of butylated hydroxytoluene (BHT) and p-methoxyphenol (PMO). Feeder layer Syrian hamster embryonic cells were co-cultured with target cells, Chinese hamster ovary cells, to promote the metabolic transformation of benzo[a]pyrene. Pretreatment with p-methoxyphenol, butylated hydroxyanisole, or butylated hydroxytoluene reduced the mutagenicity of benzo[a]pyrene in target Chinese hamster ovary cells by up to 60%. In Syrian hamster ovary cells, the tested antioxidants inhibited the metabolism of benzo[a]pyrene, leading to a decrease and a significant increase in the level of water-soluble benzo[a]pyrene glucuronide conjugates in the extracellular culture medium. Changes in intracellular monophenol levels were also observed. Because the antioxidants inhibited the production of active electrophilic benzo[a]pyrene metabolites, the binding of benzo[a]pyrene to nuclear macromolecules (especially DNA) was reduced. This study investigated the effect of two-stage treatment with p-methoxyphenol on N-methyl-N'-nitro-N-nitrosoguanidine-induced forestomach carcinoma in rats. Fifteen 6-week-old male F344 rats were divided into several groups. Each group received a single gavage administration of 150 mg/kg body weight of N-methyl-N'-nitro-N-nitrosoguanidine. One week later, they were fed a powdered diet containing 2.0%, 1.0%, 0.5%, 0.25%, or 0% p-methoxyphenol until week 52. p-Methoxyphenol induced forestomach epithelial damage and hyperplasia in a dose-dependent manner, but did not increase the incidence of any carcinogenesis, including papillary carcinoma or squamous cell carcinoma. Stimulation of cell proliferation is not necessarily associated with the promotion of the second stage of two-stage forestomach carcinogenesis. This study investigated the effects of five phenolic antioxidants on N-methyl-N-nitro-N-nitrosoguanidine (MNNG)-induced forestomach and proventricular carcinoma. Male F344 rats (n=20 per group) were used. Rats were administered 150 mg/kg body weight of N-methyl-N-nitro-N-nitrosoguanidine by gavage. One week later, they were fed diets supplemented with 0.8% catechol, 1.0% 2-tert-butyl-4-methylphenol, 1.5% p-tert-butylphenol, 1.5% methylhydroquinone, 1.5% 4-methoxyphenol, or a basal diet, respectively, for 51 weeks. A control group of 10-15 rats received no treatment. Animals were treated with N-methyl-N-nitro-N-nitrosoguanine (NMG). In NMG-treated animals, diets containing catechol (P<0.001), 2-tert-butyl-4-methylphenol (P<0.001), or p-tert-butylphenol (P<0.01) significantly increased the incidence of forestomach squamous cell carcinoma, while 4-methoxyphenol (P<0.01) inhibited carcinoma in situ. Catechol, 2-tert-butyl-4-methylphenol, p-tert-butylphenol, or 4-methoxyphenol alone induced 86.7%, 40%, 93.3%, and 100% of forestomach hyperplasia, respectively. In the pyloric region of the proventriculus, adenomatous hyperplasia and the incidence of adenocarcinoma significantly increased after N-methyl-N-nitro-N-nitrosoguanine treatment, and diets containing catechol significantly enhanced this process (P<0.001). Furthermore, treatment with catechol alone induced 100% adenomatous hyperplasia and adenocarcinoma in 20% of animals. …While some antioxidants can cause proliferation of forestomach epithelial cells and significantly enhance carcinogenesis in this tissue, others with the same or stronger proliferative potential, such as 4-methoxyphenol, may exert an inhibitory effect. Moreover, studies have shown that catechol is a known gastric gland carcinogen and strongly enhances the development of lesions induced by N-methyl-N-nitro-N-nitrosoguanine.
Chemoprophylactic effects of ascorbate palmitate (AP), carbenolide (CBX), dimethyl fumarate (DMF), and 40% and 80% of the maximum tolerated dose (MTD) levels: This study investigated the effects of dietary administration of p-methoxyphenol (p-MP) in male F344 rats during the initiation, activating, and late-activating phases of azomethane (AOM)-induced colon cancer. In a modified AIN-76A diet, the maximum tolerated doses (MTDs) of AP, CBX, DMF, and p-MP in male F344 rats were determined to be 5000, 1500, 1000, and 1000 ppm, respectively. Based on these MTD values, the carcinogenic effects of each substance at 40% and 80% MTD levels on colon cancer were tested. At 5 weeks of age, animals were divided into groups and fed either a control group (modified AIN-76A diet) or a diet containing 40% and 80% MTD levels of AP, CBX, DMF, and p-MP. At 7 weeks of age, all animals except the saline control group received subcutaneous injections of AOM twice weekly at a dose of 15 mg/kg body weight/week. All groups continued to be fed according to their respective dietary protocols until the end of the experiment 52 weeks after carcinogen treatment. Histopathological evaluation of colon tumors was performed. The results showed that dietary supplementation with AP containing 40% MTD significantly inhibited the number of non-invasive adenocarcinomas and total adenocarcinomas (invasive plus non-invasive) in the colon (tumor/animal) (P < 0.05), while 80% MTD AP significantly inhibited the incidence and number of invasive adenocarcinomas and total adenocarcinomas in the colon (percentage of tumors in animals) (P < 0.01). Dietary supplementation with CBX containing 40% and 80% MTD inhibited the incidence and number of invasive adenocarcinomas and total adenocarcinomas (P < 0.05 to 0.001), while 40% and 80% MTD DMF and p-MP significantly inhibited the incidence and number of invasive adenocarcinomas (P < 0.05 to 0.001). However, DMF and p-MP had no significant effect on the incidence and number of non-invasive adenocarcinomas and total adenocarcinomas (P > 0.05). These results suggest that AP and CBX possess potential chemopreventive properties for colon cancer. For more complete data on interactions of 4-methoxyphenols (11 in total), please visit the HSDB record page.

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Non-human toxicity values
Rats oral LD50 1600 mg/kg
Mouse intraperitoneal LD50 250 mg/kg
Rabbit intraperitoneal LD50 720-790 mg/kg

[1]. Postinflammatory hyperpigmentation: etiologic and therapeutic considerations. Am J Clin Dermatol. 2011 Apr 1;12(2):87-99.

[2]. Carcinogenicity of antioxidants BHA, caffeic acid, sesamol, 4-methoxyphenol and catechol at low doses, either alone or in combination, and modulation of their effects in a rat medium-term multi-organ carcinogenesis model. Carcinogenesis. 1998 Jan;19(1):207-12.

[3]. Increase in the levels of chaperone proteins by exposure to beta-estradiol, bisphenol A and 4-methoxyphenol in human cells transfected with estrogen receptor alpha cDNA. Toxicol In Vitro. 2009 Jun;23(4):728-35.

Therapeutic Uses
Anti-tumor drugs; antioxidants. Pigmentation disorders, especially hyperpigmentation, are a major concern for people with darker skin tones. Pigmentation disorders such as melasma and post-inflammatory hyperpigmentation (PIH) can cause psychological and emotional distress and negatively impact a patient's health-related quality of life. The exact causes of these disorders are unknown. Treatments for melasma and PIH target different stages in the melanin production and degradation cycle. Treatments include topical medications and skin regeneration surgery. Hydroquinone remains the gold standard for topical medications. Other effective medications include kojic acid, azelaic acid, hydroquinone, and retinoids. Cosmetic ingredients include licorice, arbutin, soy, N-acetylglucosamine, and niacinamide. Skin remodeling therapies for melasma and post-inflammatory hyperpigmentation (PIH) include chemical peels, microdermabrasion, lasers, and intense pulsed light (IPL). These therapies are best used in conjunction with topical whitening agents. Given that darker skin is more prone to pigmentation, skin remodeling therapies should be used with caution. Repeated superficial skin remodeling therapies yields the best results. In addition, UV protection measures, such as the use of broad-spectrum sunscreen, are crucial for the successful treatment of these conditions. Post-inflammatory hyperpigmentation (PIH) is a reactive hyperpigmentation that is a sequela of various inflammatory skin diseases. PIH can negatively impact a patient's quality of life, especially for those with darker skin. Studies show that pigmentary abnormalities, including PIH, are among the most common complaints when people with darker skin visit dermatologists. This is likely due to unstable melanocytes producing or depositing excessive amounts of melanin in the epidermis or dermis. Various endogenous or exogenous inflammations can lead to post-inflammatory hyperpigmentation (PIH). Typically, most epidermal lesions are tan, brown, or dark brown, while dermal hyperpigmentation is bluish-gray. Depigmenting agents target different steps in melanin production, most commonly inhibiting tyrosinase. These medications include hydroquinone, azelaic acid, kojic acid, arbutin, and certain licorice extracts. Other medications include retinoic acid, hydroquinone, ascorbic acid (vitamin C), nicotinamide, N-acetylglucosamine, and soy, which work through different mechanisms of depigmentation. Certain treatments are also effective for PIH, such as chemical peels and laser therapy. It is worth noting that these treatments may also lead to post-inflammatory hyperpigmentation (PIH). Finally, cosmetic concealing therapy may offer some improvement for lesions that are not suitable for drug or surgical treatment.
The safety and efficacy of Solage solution in the prevention or treatment of melasma or post-inflammatory hyperpigmentation have not been established. /US product label contains/ /Solage/
For more complete data on the therapeutic uses of 4-methoxyphenol (of 9), please visit the HSDB record page.

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Drug Warnings
This product is contraindicated in patients with known hypersensitivity to methoxyphenol, retinoic acid, or any ingredient in this formulation. /Solage/
Because retinoic acid can severely irritate eczematous skin, patients with eczema should use methoxyphenol and retinoic acid with extreme caution. In addition, hydroquinone and retinoic acid are both skin irritants, and the risk of long-term sequelae after continuous skin irritation for more than 52 weeks is unclear. Skin irritation caused by this drug may lead to increased responsiveness to environmental stimuli such as wind, sun exposure, and cold. If local irritation is severe, temporary or permanent discontinuation or dose reduction should be considered. /Solage/
The safety and efficacy of hydroquinone and retinoic acid in patients with moderate or severe hyperpigmentation have not been established. /Solage/
Patients with a personal or family history of vitiligo may have an enhanced response to topical hydroquinone and retinoic acid solutions. In a clinical trial, a patient with a family history of vitiligo developed hypopigmentation in untreated areas, with some areas continuing to worsen for at least one month after discontinuation of the drug; after 6 weeks of treatment, the hypopigmentation symptoms were reduced, and some lesions disappeared on day 106 of treatment, but not all lesions disappeared. /Solage/
For more complete data on drug warnings for 4-methoxyphenol (13 in total), please visit the HSDB record page.

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Pharmacodynamics
In fact, hydroquinone is considered a melanocyte-toxic chemical that, upon oxidation in melanocytes, forms toxic substances such as quinones. These cytotoxic compounds can subsequently damage and destroy pigment cells, leading to skin depigmentation. In response, skin cells naturally possess the ability to protect themselves from such cytotoxic substances, thanks to the detoxification effects of endogenous intracellular glutathione and glutathione S-transferase on these cytotoxic compounds. Nevertheless, the mechanism of action of hydroquinone is sometimes described precisely through these seemingly negative and harmful pharmacodynamic characteristics.

C7H8O2

124.1372

124.052

150-76-5

Mequinol-d4;126840-02-6

9015

White to light brown solid powder

1.1±0.1 g/cm3

243.0±0.0 °C at 760 mmHg

56 °C

120.8±4.8 °C

0.0±0.5 mmHg at 25°C

1.535

1.31

1

2

1

9

75

0

NWVVVBRKAWDGAB-UHFFFAOYSA-N

InChI=1S/C7H8O2/c1-9-7-4-2-6(8)3-5-7/h2-5,8H,1H3

4-methoxyphenol

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)

H2O : ≥ 100 mg/mL (~805.54 mM)
DMSO : ≥ 100 mg/mL (~805.54 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (20.14 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 25.0 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: ≥ 2.5 mg/mL (20.14 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 25.0 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: ≥ 2.5 mg/mL (20.14 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 25.0 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.)