Androgen Receptor

Testosterone is a steroid sex hormone indicated to treat primary hypogonadism and hypogonadotropic hypogonadism. Testosterone antagonizes the androgen receptor to induce gene expression that causes the growth and development of masculine sex organs and secondary sexual characteristics. Testosterone was isolated from samples and also synthesized in 1935.

Testosterone antagonizes the androgen receptor to induce gene expression that causes the growth and development of masculine sex organs and secondary sexual characteristics. The duration of action of testosterone is variable from patient to patient with a half life of 10-100 minutes. The therapeutic index is wide considering the normal testosterone levels in an adult man range from 300-1000ng/dL. Counsel patients regarding the risk of secondary exposure of testosterone topical products to children.

Absorption, Distribution and Excretion
A single 100mg topical dose of testosterone has an AUC of 10425±5521ng\*h/dL and a Cmax of 573±284ng/dL. Testosterone is approximately 10% bioavailable topically.
90% of an intramuscular dose is eliminated in urine, mainly as glucuronide and sulfate conjugates. 6% is eliminated in feces, mostly as unconjugated metabolites.
The volume of distribution of testosterone in elderly men is 80.36±24.51L.
The mean metabolic clearance in middle aged men is 812±64L/day.
Testosterone is absorbed systemically through the skin following topical application as a gel or transdermal system. Following topical application of a hydroalcoholic gel formulation of testosterone (AndroGel, Testim) to the skin, the gel quickly dries on the skin surface, which serves as a reservoir for sustained release of the hormone into systemic circulation. Approximately 10% of a testosterone dose applied topically to the skin as a 1% gel is absorbed percutaneously into systemic circulation. The manufacturer of AndroGel states that increases in serum testosterone concentrations were apparent within 30 minutes of topical application of a 100-mg testosterone dose of the 1% gel, with physiologic concentrations being achieved in most patients within 4 hours (pretreatment concentrations were not described); percutaneous absorption continues for the entire 24-hour dosing interval. Serum testosterone concentrations approximate steady-state levels by the end of the initial 24 hours and are at steady state by the second or third day of dosing of the 1% gel. With daily topical application of the 1% gel (AndroGel), serum testosterone concentrations 30, 90, and 180 days after initiating treatment generally are maintained in the eugonadal range. Administration of 10 or 5 g of AndroGel daily results in average daily serum testosterone concentrations of 794 or 566 ng/dL, respectively, at day 30. Following discontinuance of such topical therapy, serum testosterone concentrations remain within the normal range for 24-48 hours but return to pretreatment levels by the fifth day after the last application.
With topical application of a transdermal preparation, the extent of percutaneous testosterone absorption varies according to the site of application, possibly secondary to regional differences in skin permeability, cutaneous blood flow, and/or degree of adhesion between the transdermal system and skin. In one study in which transdermal systems were applied to the abdomen, back, chest, shin, thigh, or upper arm, serum hormone profiles were qualitatively similar with each site, but steady-state serum concentrations showed significant differences, decreasing in order with the back, thigh, upper arm, abdomen, chest, and shin. Application of Androderm transdermal systems to the abdomen, back, thighs, or upper arms results in achievement of similar serum testosterone concentration profiles, and these sites are recommended as optimal for rotation of application sites during chronic therapy. Daily nighttime (at approximately 10 p.m.) application of Androderm transdermal system results in a serum testosterone concentration profile that mimics the endogenous diurnal pattern in healthy young men. In one study, showering 3 hours after application of Androderm decreased peak plasma concentrations of testosterone by 0.4% compared with not showering 3 hours after application of the transdermal system. In addition, showering 3 hours after transdermal system application did not substantially alter the systemic exposure of testosterone.
Following topical application of transdermal systems of testosterone, the hormone is absorbed percutaneously into systemic circulation. Although interindividual variation in percutaneous testosterone absorption occurs, serum testosterone concentrations achieved with recommended dosages of transdermal systems of the drug generally reach the normal range during the first day of dosing and are maintained during continuous dosing without accumulation. Average daily serum testosterone concentrations in patients receiving Androderm reportedly are 498 ng/dL at steady state. Mean ratios of testosterone to DHT are within the normal range.
Esterification of testosterone generally results in less polar compounds. The enanthate ester of testosterone is absorbed slowly from the lipid tissue phase at the IM injection site, achieving peak serum concentrations about 72 hours after IM injection; thus, this preparation has a prolonged duration of action (i.e., up to 2-4 weeks) following IM administration. Because IM injection of testosterone esters causes local irritation, the rate of absorption may be erratic. /Testosterone esters/
For more Absorption, Distribution and Excretion (Complete) data for Testosterone (9 total), please visit the HSDB record page.

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Metabolism / Metabolites
Testosterone is metabolized to 17-keto steroids through two different pathways. The major active metabolites are estradiol and dihydrotestosterone (DHT). Testosterone can be hydroxylated at a number of positions by CYP3A4, CYP2B6, CYP2C9, and CYP2C19; glucuronidated by UGT2B17; sulfated; converted to estradiol by aromatase; converted to dihydrotestosterone (DHT) by 5α-reductase; metabolized to androstenedione by CYP3A4, CYP2C9, and CYP2C19; or converted to DHT glucuronide. Androstenedione undergoes metabolism by aromatase to form estrone, which undergoes a reversible reaction to form estradiol. Androstenedione can also be converted to 5α-androstanedione by 5α-reductase, which can be further metabolized to 5α-androsterone. DHT can be glucuronidated or sulfated, or metabolized to 5α-androstanediol, androstane-3α,17β-diol, or androstane-3β,17β-diol. DHT can also be reversibly converted to 5α-androstanedione.
Extensive reductive metabolism of testosterone occurs not only in the liver, but also in a variety of extrahepatic tissues, especially in target organs of the sex hormones; the ultimately effective physiological androgen is formed in the target tissues. Testosterone metabolism occurs not only in the prostate and seminal vesicles but also in rat uterus, rabbit placenta, rodent testis and primate brain. In rats, the small intestine is also capable of metabolizing testosterone.
It is transformed to 5-alpha-dehydrotestosterone in target organs such as the prostate, sebaceous glands and seminal vesicles; only the latter compound binds to the androgen-receptor site in these target organs.
Large quantitative differences in testosterone metabolism are evident between female and male rats. The reason for this phenomenon is that many steroid-metabolizing enzymes in rats are either androgen- or estrogen-dependent; the sex hormones thus act in an inductive or a repressive manner.
Esters of testosterone, such as the propionate, the heptanoate, the cypionate, the valerate, the isovalerate, the enanthate and the undecanoate, are partially cleaved in vivo to release the parent compound. This has been demonstrated by oral administration of testosterone undecanoate in oily solution to rats: most of the compound is converted within the intestinal wall, the first step being partial splitting off of the fatty acid moiety. The non-metabolized portion, however, and the metabolite 5-alpha-dihydrotestosterone undecanoate, are absorbed via the lymphatic system and made available for androgenic action to the organism. /Testosterone esters/
For more Metabolism/Metabolites (Complete) data for Testosterone (6 total), please visit the HSDB record page.
Testosterone has known human metabolites that include 2beta-Hydroxytestosterone, Androstenedione, 16beta-Hydroxytestosterone, 6alpha-Hydroxytestosterone, 15beta-Hydroxytestosterone, 15-Hydroxytestosterone, Testosterone sulfate, 16-Hydroxytestosterone, and 2alpha-Hydroxytestosterone.
Testosterone is metabolized to 17-keto steroids through two different pathways. The major active metabolites are estradiol and dihydrotestosterone (DHT).
Route of Elimination: About 90% of a dose of testosterone given intramuscularly is excreted in the urine as glucuronic and sulfuric acid conjugates of testosterone and its metabolites; about 6% of a dose is excreted in the feces, mostly in the unconjugated form.
Half Life: 10-100 minutes

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Biological Half-Life
The half life of testosterone is highly variable, ranging from 10-100 minutes.
The plasma half-life of testosterone reportedly ranges from 10-100 minutes. The plasma half-life of testosterone cypionate after IM injection is approximately 8 days. Following removal of an Androderm transdermal system, plasma testosterone concentrations decline with an apparent half-life of approximately 70 minutes ... .

Toxicity Summary
IDENTIFICATION AND USE: Testosterone is an anabolic steroid for systemic use. It consists of odorless or almost odorless crystals or crystalline powder. Naturally-occuring anabolic steroids are synthesized in the testis, ovary and adrenal gland. Anabolic steroids are listed as Schedule III controlled substances. HUMAN EXPOSURE AND TOXICITY: The main risks associated with testosterone are those of excessive androgens: menstrual irregularities and virilization in women and impotence, premature cardiovascular disease and prostatic hypertrophy in men. Both men and women can suffer liver damage with oral anabolic steroids containing a substituted 17-alpha-carbon. Psychiatric changes can occur during use or after cessation of these agents. Acute overdosage can produce nausea and gastrointestinal upset. Chronic usage is thought to cause an increase in muscle bulk, and can cause an exaggeration of male characteristics and effects related to male hormones. There is no clear evidence that anabolic steroids enhance overall athletic performance. Precocious prostatic cancer has been described after long-term anabolic steroid abuse. Cases where hepatic cancers have been associated with anabolic steroid abuse have been reported. Testosterone may cause fetal harm when administered to pregnant women due to the potential for virilization of a female fetus. Androgenic effects including clitoral hypertrophy, labial fusion of the external genital fold to form a scrotal-like structure, abnormal vaginal development, and persistence of a urogenital sinus have occurred in the female offspring of women who were given androgens during pregnancy. The degree of masculinization is related to the amount of drug given to the woman and the age of the fetus; masculinization is most likely to occur in a female fetus when exposure to androgens occurs during the first trimester. ANIMAL STUDIES: The effect of testosterone on the prostate of castrated rats was described as a significant increase in prostatic weight which occurred after 6 wk treatment with testosterone. In female mice injected subcutaneously with 25 ug testosterone daily for the first five days after birth, 7/9 developed hyperplastic epithelial lesions, resembling epidermoid carcinomas at about 71 weeks of age. Chronic treatment of rats with testosterone produced a low prostate carcinoma incidence. A high carcinoma incidence can only be produced by chronic treatment with testosterone following administration of carcinogens. Daily subcutaneous injections for 4-8 days of total doses of 0.5-80 mg testosterone into rats between days 10 and 20 of gestation and of total doses of 1-55 mg testosterone propionate between days 12 and 19 of gestation resulted in resorptions, necrosis, lethality, post-partum mortality and various degrees of masculinization in female offspring. Deposteron (testosterone cypionate) was genotoxic and cytotoxic in mice. Testosterone acted both as a mitogenic and genotoxic agent in L929 cells.
Testosterone is considered an anabolic steroid. It plays a key role in the development of male reproductive tissues such as the testis and prostate as well as promoting secondary sexual characteristics such as increased muscle, bone mass, and the growth of body hair. High levels of testosterone can lead to masculinization in females or premature puberty in young boys. Chronically high levels in adults increase the incidence of heart attack, stroke and blood clots by lowering the level of HDL (good cholesterol) and increasing the level of LDL (bad cholesterol). Chronic high use of anabolic steroids (such as testosterone) appears to lead to cardiac myopathy and weakening the left ventricle. The development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), arises because of increased conversion of testosterone to estradiol by the enzyme aromatase. Reduced sexual function and temporary infertility can also occur in males.
The mechanism of testosterone’s action is as follows: Free testosterone is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5-alpha reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of testosterone. Once bound, the ligand-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Limited data indicate that a low-dose (100 mg) subcutaneous testosterone pellet given to a nursing mother appears not to increase milk testosterone levels markedly. Subcutaneous testosterone cypionate does increase milk testosterone levels. However, testosterone has low oral bioavailability because of extensive first-pass metabolism, so it appears to not increase serum testosterone levels in breastfed infants. Breastfed infants appear not to be adversely affected by maternal or transgender paternal testosterone therapy. High doses of testosterone can suppress lactation.
◉ Effects in Breastfed Infants
After implantation of a 100 mg pellet of testosterone subcutaneously in a postpartum mother, her infant (age not stated) was breastfed (extent not stated). No adverse effects were noted in the infant over a 5-month period.
A transgender male began receiving subcutaneous testosterone cypionate 50 mg weekly 13.75 months after giving birth. The dose was increased to 80 mg weekly after 1 month. His male infant was partially “chestfed” (extent not stated) until the infant self-weaned at 137 days after initiation of testosterone (18 months of age). During this time, no adverse events or signs of virilization were noted by the infant’s pediatrician. The infant grew and developed normally.
◉ Effects on Lactation and Breastmilk
Supraphysiologic serum levels of testosterone, either from a tumor or from exogenously administered testosterone, reduces milk production in postpartum women. Testosterone alone reduces serum prolactin; however, when given in combination with estrogen and progestin, serum prolactin levels are not markedly reduced. Testosterone was previously used therapeutically to suppress lactation, usually in combination with an estrogen.

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Protein Binding
Testosterone is 40% bound to sex hormone binding globulin, 2% unbound, and the remainder is bound to albumin and other proteins.

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Interactions
Concomitant use of anabolic androgenic steroids and cocaine has increased in the last years. However, the effects of chronic exposure to these substances during adolescence on cardiovascular function are unknown. Here, we investigated the effects of treatment for 10 consecutive days with testosterone and cocaine alone or in combination on basal cardiovascular parameters, baroreflex activity, hemodynamic responses to vasoactive agents, and cardiac morphology in adolescent rats. Administration of testosterone alone increased arterial pressure, reduced heart rate (HR), and exacerbated the tachycardiac baroreflex response. Cocaine-treated animals showed resting bradycardia without changes in arterial pressure and baroreflex activity. Combined treatment with testosterone and cocaine did not affect baseline arterial pressure and HR, but reduced baroreflex-mediated tachycardia. None of the treatments affected arterial pressure response to either vasoconstrictor or vasodilator agents. Also, heart to body ratio and left and right ventricular wall thickness were not modified by drug treatments. However, histological analysis of left ventricular sections of animals subjected to treatment with testosterone and cocaine alone and combined showed a greater spacing between cardiac muscle fibers, dilated blood vessels, and fibrosis. These data show important cardiovascular changes following treatment with testosterone in adolescent rats. However, the results suggest that exposure to cocaine alone or combined with testosterone during adolescence minimally affect cardiovascular function.
Topical administration of 0.1% triamcinolone cream prior to application of a testosterone transdermal system did not alter absorption of testosterone; however, pretreatment with topical administration of triamcinolone ointment substantially reduced absorption of testosterone.
Administration of IM testosterone cypionate resulted in increased clearance of propranolol in one study. It is not known whether there is a potential for this interaction with topically administered testosterone gel. /Testosterone cypionate/
Testosterone may potentiate the action of oral anticoagulants, causing bleeding in some patients. When testosterone therapy is initiated in patients receiving oral anticoagulants, dosage reduction of the anticoagulant may be required to prevent an excessive hypoprothrombinemic response. In patients receiving concomitant therapy with testosterone and anticoagulants, more frequent monitoring of INR and prothrombin time is recommended, especially during initiation or discontinuance of therapy.
For more Interactions (Complete) data for Testosterone (10 total), please visit the HSDB record page.

[1]. https://pubchem.ncbi.nlm.nih.gov/compound/6013

Therapeutic Uses
Androgens
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Testosterone is included in the database.
In males, testosterone is used for the management of congenital or acquired primary hypogonadism such as that resulting from orchiectomy or from testicular failure caused by cryptorchidism, bilateral torsion, orchitis, or vanishing testis syndrome. Testosterone also is used in males for the management of congenital or acquired hypogonadotropic hypogonadism such as that resulting from idiopathic gonadotropin or gonadotropin-releasing hormone (luteinizing hormone releasing hormone) deficiency or from pituitary-hypothalamic injury caused by tumors, trauma, or radiation. If any of these conditions occur before puberty, androgen replacement therapy will be necessary during adolescence for the development of secondary sexual characteristics and prolonged therapy will be required to maintain these characteristics. Prolonged androgen therapy also is required to maintain sexual characteristics in other males who develop testosterone deficiency after puberty. /Included in US product labeling/
When the diagnosis is well established, testosterone may be used to stimulate puberty in carefully selected males with delayed puberty. These males usually have a family history of delayed puberty that is not caused by a pathologic disorder. Brief treatment with conservative doses of an androgen may occasionally be justified in these males if they do not respond to psychologic support. Because androgens may adversely affect bone maturation in these prepubertal males, this potential risk should be fully discussed with the patient and his parents prior to initiation of androgen therapy. If androgen therapy is initiated in these prepubertal males, radiographs of the hand and wrist should be obtained at 6-month intervals to determine the effect of therapy on the epiphyseal centers. Testosterone is designated an orphan drug by the FDA for use in this condition. /Included in US product labeling/
For more Therapeutic Uses (Complete) data for Testosterone (17 total), please visit the HSDB record page.

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Drug Warnings
/BOXED WARNING/ WARNING: SECONDARY EXPOSURE TO TESTOSTERONE. Virilization has been reported in children who were secondarily exposed to testosterone gel. Children should avoid contact with unwashed or unclothed application sites in men using testosterone gel. Healthcare providers should advise patients to strictly adhere to recommended instructions for use.
Cardiovascular events, including MI or stroke, have been reported during postmarketing experience with testosterone transdermal system (Androderm). Testosterone should be used with caution in patients at high risk for cardiovascular disease (e.g., older men, those with diabetes mellitus or obesity). Patients should be advised to immediately report symptoms suggestive of MI or stroke (e.g., chest pain, shortness of breath, unilateral weakness, difficulty talking) to their clinician.
Venous thromboembolic events, including deep-vein thrombosis (DVT) and pulmonary embolism (PE), have been reported during postmarketing experience with testosterone preparations, including testosterone transdermal system (Androderm). Patients reporting symptoms of pain, edema, warmth, and erythema in a lower extremity or presenting with acute shortness of breath should be evaluated for possible DVT or PE, respectively. If venous thromboembolism is suspected, testosterone therapy should be discontinued and appropriate evaluation and management should be initiated.
Testosterone should be used with caution in patients with cardiac, renal, and/or hepatic dysfunction since edema may occur as a result of sodium and water retention. Edema, with or without congestive heart failure, may be a serious complication in patients with preexisting cardiac, renal, and/or hepatic disease. If edema occurs during testosterone therapy and it is considered a serious complication, the drug should be discontinued; diuretic therapy may also be necessary.
For more Drug Warnings (Complete) data for Testosterone (34 total), please visit the HSDB record page.

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Pharmacodynamics
Testosterone antagonizes the androgen receptor to induce gene expression that causes the growth and development of masculine sex organs and secondary sexual characteristics. The duration of action of testosterone is variable from patient to patient with a half life of 10-100 minutes. The therapeutic index is wide considering the normal testosterone levels in an adult man range from 300-1000ng/dL. Counsel patients regarding the risk of secondary exposure of testosterone topical products to children.

C19H28O2

288.43

288.208

58-22-0

6013

White needles from dilute acetone
Needles from dilute acetone
White or slightly cream-white crystals or crystalline powder

1.1±0.1 g/cm3

432.9±45.0 °C at 760 mmHg

152-156 °C

184.7±21.3 °C

0.0±2.3 mmHg at 25°C

1.560

3.47

1

2

0

21

508

6

C[C@@]12CCC(=O)C=C2CC[C@H]3[C@@H]4CC[C@@H]([C@@]4(C)CC[C@@H]31)O

MUMGGOZAMZWBJJ-DYKIIFRCSA-N

InChI=1S/C19H28O2/c1-18-9-7-13(20)11-12(18)3-4-14-15-5-6-17(21)19(15,2)10-8-16(14)18/h11,14-17,21H,3-10H2,1-2H3/t14-,15-,16-,17-,18-,19-/m0/s1

(8R,9S,10R,13S,14S,17S)-17-hydroxy-10,13-dimethyl-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthren-3-one

Primotest; Homosteron; Testosterone; testosterone; 58-22-0; Testosteron; Androderm; Testim; Homosterone; Virosterone; Testiculosterone;

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.)