57-85-2 Usage
Uses
Used in Human Medicine:
Testosterone propionate is used as a medication for the treatment of low testosterone levels in men, particularly in cases of hypogonadism or andropaus. It is also used to treat anemia accompanying renal and bone marrow failure, endometriosis, cancer, and wasting syndrome in human immunodeficiency virus infection. Additionally, it is utilized in the treatment of catabolic states and cachexia, corticosteroid therapy, osteoporosis, growth stimulation in male puberty, prophylaxis for hereditary angioedema, hepatic disease, and female to male transsexualism, hypoplastic anemia, multiple sclerosis, sexual dysfunction, and depression.
Used in Veterinary Medicine:
Testosterone propionate is used in veterinary medicine to treat chronic wasting conditions and improve appetite and physical appearance in animals. It is available in various pharmaceutical formulations and is also used in the form of testosterone ester preparations in oil and testosterone suspension in aqueous vehicles.
Used in Athletic Performance Enhancement:
Testosterone propionate is used as a performance-enhancing drug by athletes and bodybuilders to increase strength, lean body mass, and muscle size. It is particularly popular for its ability to improve physical appearance and body image.
Used in Research:
Testosterone propionate is also used in research settings to study its effects on various subjects, such as pregnant ewes, in order to better understand its impact on different physiological processes.
Used in Muscle Mass Building:
Testosterone propionate is used as a muscle mass building agent, particularly for individuals seeking to enhance their physical performance and appearance. It is commonly utilized by bodybuilders and athletes for this purpose.
Used in Animal Agriculture:
Testosterone propionate is used in heifers to stimulate maximal growth, making it an important tool in the animal agriculture industry for improving the overall health and productivity of livestock.
Pharmacodynamics
The administration of testosterone propionate can induce production of proteins related to male sexual development. On the other hand, testosterone itself present an estrogenic activity due to interaction with aromatase enzyme, thus the continuous administration of testosterone propionate may cause the elevation of plasma estrogen. Clinical trials showed as well, a decrease in plasma LH after testosterone propionate administration[13].
Mode of action
Anabolic steroids are thought to exert their actions by several different mechanisms. These mechanisms include modulating androgen receptor expression as a consequence of[i] intracellular metabolism and by[ii] directly affecting the topology of the androgen receptor and thus subsequent interaction with co-activators and transcriptional activity. Other mechanisms include[iii] an anticatabolic effect by interfering with glucocorticoid receptor expression; and[iv] by non-genomic, as well as by genomic pathways, in the CNS resulting in behavioural changes. These mechanisms are discussed herein. Free testosterone[T] is transported into the cytoplasm of target tissue cells, further binding to the androgen receptor, or being reduced to 5alpha-dihydrotestosterone(DHT) by the cytoplasmic enzyme 5alpha-reductase. The binding areas are called hormone response elements(HREs), and influence transcriptional activity of certain genes, producing the androgen effects.[14-16]
Mode of action
Testosterone Propionate is a short acting oil-based injectable formulation of testosterone. Testosterone inhibits gonadotropin secretion from the pituitary gland and ablates estrogen production in the ovaries, thereby decreasing endogenous estrogen levels. In addition, this agent promotes the maintenance of male sex characteristics and is indicated for testosterone replacement in hypogonadal males.
The relation to obesity
Several studies have demonstrated an inverse relationship between indicators of obesity(body mass index, waist circumference, a reliable indicator of visceral obesity), and testosterone levels over all age groups[15-17]. Obesity contributes to onset of type II diabetes mellitus(T2DM), dyslipidemia, hypertension and, therefore, MetS. An inverse association between the severity of features of MetS, T2DM and plasma testosterone has been previously reported[18]. In one study, this association was independent of age and body mass index[19], underlining the complexity of the relationship between testosterone and obesity[20]. This became also apparent from another study that verified the prevalence of low testosterone levels in male T2DM patients, related to variations in BMI, waist circumference, neuropathy, triglycerides, CRP, glucose, insulin and HOMAIR, but no increase of silent myocardial ischemia or peripheral arterial disease was established[21]. This is supported by other studies linking low testosterone, cardiovascular risk and insulin resistance(for review[22]). Although age is associated with the prevalence of MetS, young men with features of the MetS exhibit reduced testosterone levels[23, 24] and testosterone treatment in these individuals positively affects weight reduction, with concomitant reduction in insulin resistance(IR). The exact pathophysiological mechanisms responsible for reduced testosterone levels in obesity remain under investigation[15], however, hyperinsulinemia is shown to suppress serum testosterone levels[25]. Testosterone levels are reduced in men with T2DM, with an inverse association between testosterone levels and glycosylated hemoglobin(HbA1c)[26] and this occurs independently of medications, such as statins[27]. In men with low plasma testosterone, the likelihood of T2DM is increased and several large prospective studies have shown that low T testosterone levels predict development of T2DM in men. Low levels of testosterone are associated with a decreased lean body mass, and relative muscle mass is inversely associated with insulin resistance and prediabetes[28].
Adverse reactions and precaution
Testosterone propionate is a kind of AAS. The most common reversible side effect of AAS is cosmetic in nature. The orally used AAS may cause hepatotoxicity. However there is no report describing hepatotoxicity due to use of parenteral AAS preparations, which appear to damage heart muscles in long-term use[29]. There are several side effects of AAS use such as; headaches, gastrointestinal irritation, fluid retention in the extremities, diarrhea, stomach pains, oily skin. Additionally jaundice, menstrual abnormalities, hypertension and infections at injection site may be observed. Acne develops in both sexes at puberty during treatment with AAS due to secretion of the natural oil sebum and growth of sebaceous glands[30]. Males using high doses of AAS may have elevated circulating estrogen levels similar to women during a normal menstral cycle. This effect is result of aromatization of testosterone in part to estrogens. Therefore, gynecomastia and breast pain may be observed in men taking high doses of AAS[31].
Chronic adverse effects associated with AAS abuse include acne, urogenital problems, endocrine abnormalities, neuropsychiatric disorders, hepatic and cardiovascular diseases. Acne is common adverse effect of AAS use seen in almost 50% of the androgen uses. Acne fulminans and acne conglobata are the most common forms of acne associated with AAS[32]. Subjects using AAS should be warned that acne associated with AAS can get worse with vitamin B supplement[32]. Gynecomastia and suppression of spermatogenesis are frequent consequences of AAS use. High dose of AAS suppresses the hypothalamic-pituitary-gonadal axis due to negative feedback and, it may take weeks or months for the axis to recover. Consequently atrophy of the seminiferous tubules during this time may result in subfertility or infertility[33]. Furthermore, subjects may continue to encounter symptoms of hypogonadism[erectile dysfunction, low libido and low vitality] even after discontinuation of AAS until the axis recovers. Recent reports suggest that use of clomiphene citrate may hasten the recovery of gonadal axis[34].
World Health Organization (WHO)
In 1982, low dosage preparations of testosterone propionate, a
synthetic ester of the naturally-occurring androgen, testosterone, were prohibited
in Bangladesh following their inadmissable promotion as anabolic agents for use
in malnourished children. Higher dosage preparations of testosterone propionate
remain available in many countries, including Bangladesh, for several highly
specific but limited indications including hypogonadism and the palliative
treatment of inoperable breast cancer.
Air & Water Reactions
Insoluble in water.
Reactivity Profile
Testosterone propionate is sensitive to light. Incompatible with alkalis and oxidizing agents. .
Fire Hazard
Flash point data for Testosterone propionate are not available; however, Testosterone propionate is probably combustible.
Biochem/physiol Actions
Androgens direct the development of the male phenotype during embryogenesis and at puberty. Testosterone is an androgen that is secreted by the testis. This hormone is converted to dihydrotestosterone in the target tissues where it regulates several biological functions. Testosterone propionate has been synthetically derived from a plant. This product has extended and faster-acting functions when compared to other testosterone esters.
Safety Profile
with experimental neoplastigenic, tumorigenic, and teratogenic data. Moderately toxic by ingestion and wintraperitoneal routes. Human male reproductive effects by intramuscular and parenteral routes: changes in spermatogenesis, testes, epid~dpmis, and sperm duct. Human female reproductive effects by intramuscular and parenteral routes: menstrual cycle changes or disorders and effects on ferthty. Experimental reproductive effects. Mutation data reported. When heated to decomposition it emits acrid smoke and irritating fumes. See also TESTOSTERONE.
Purification Methods
Crystallise the propionate from aqueous EtOH, or Et2O/pet ether (m 121o), and it has max at 240nm (EtOH), and [] 20 +114o (c 1, CHCl3). Also purify it by HPLC. [Ercol & de Ruggieri J Am Chem Soc 75 650, 652 1953, polymorphism: Brandst.tter-Kuhnert & Kofler Mickokim Acta 847, 850 1959, Beilstein 8 IV 977.]
Check Digit Verification of cas no
The CAS Registry Mumber 57-85-2 includes 5 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 2 digits, 5 and 7 respectively; the second part has 2 digits, 8 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 57-85:
(4*5)+(3*7)+(2*8)+(1*5)=62
62 % 10 = 2
So 57-85-2 is a valid CAS Registry Number.
InChI:InChI=1/C22H32O3/c1-4-20(24)25-19-8-7-17-16-6-5-14-13-15(23)9-11-21(14,2)18(16)10-12-22(17,19)3/h13,16-19H,4-12H2,1-3H3/t16?,17?,18?,19-,21-,22-/m0/s1
57-85-2Relevant articles and documents
Preparation method of alkyl acid testosterone
-
Paragraph 0020-0021, (2020/11/10)
The invention discloses a preparation method of alkyl acid testosterone, and belongs to the technical field of medicine preparation and processing. According to the method, testosterone serves as a raw material and is esterified into testosterone ester, a solvent used in the esterification reaction is a non-water-soluble organic solvent, the amount of wastewater is reduced, the solvent can be recycled, and the process is more environmentally friendly. The method is high in yield, the total molar yield of the final product is higher than 85%, and the method has extremely high commercial competitiveness, is suitable for industrial large-scale production and has good economic benefits.
Synthesis method of alkyl acid testosterone
-
, (2020/12/10)
The invention discloses a synthesis method of alkyl acid testosterone, and belongs to the technical field of synthesis and processing of medicines. The method comprises the following steps of: taking4-androstenedione (4AD) as an initial raw material, firstly, carrying out enol ether protection on the keto group at the site 3, and reducing carbonyl at the site 17 into hydroxyl; or taking 4-androstenedione (4AD) as an initial raw material, firstly carrying out enol ether protection on the keto group at the site 3, then reducing carbonyl at the site 17 into hydroxyl, then carrying out hydrolysison the site 3 to obtain testosterone, and carrying out esterification and third-site hydrolysis to obtain the testosterone ester after testosterone third-site ketal protection. According to the method disclosed by the invention, the third site is protected during esterification reaction, the generation of impurities can be reduced, and an esterification reaction solvent is a water-insoluble organic solvent, so that after the reaction is completed, products can be directly extracted in a layered manner, a large amount of water does not need to be added to separate out the products, the amountof wastewater is reduced, the solvent can be recycled, and the process is more suitable for industrial production.
Highly efficient, solvent-free esterification of testosterone promoted by a recyclable polymer-supported tosylic acid catalyst under microwave irradiation
Borowiecki, Pawe?,Kraszewski, Maciej
, p. 288 - 305 (2020/02/13)
Although the classical acylation of testosterone clearly benefits from a broad substrate scope and available catalysts, the requirement of hazardous reagents and the high waste production are its drawbacks. To optimize the process efficiency as well as minimize the environmental impact, we decided to develop a novel method of testosterone esters synthesis, which relies on the usage of recyclable heterogeneous polymer-supported tosylic acid catalyst and microwave-assistance effect in a non-solvent system. Under the established MW-conditions, the acceleration of the process rate was so efficient that the reaction completed within 2.5 min, thus affording the desired esters in the 33–96% yield range without using a work-up procedure. Furthermore, the elaborated catalytic system could be recycled for at least 2 runs not only without a loss of the products yield, but unexpectedly with significant improvement of the reaction efficiency, which may indicate that the reduction of the catalyst loading is possible. We believe that this finding constitutes a very good starting-point for further optimization of the studied process.
Dehalogenation of vicinal dihalo compounds by 1,1′-bis(trimethylsilyl)-1: H,1′ H-4,4′-bipyridinylidene for giving alkenes and alkynes in a salt-free manner
Rej, Supriya,Pramanik, Suman,Tsurugi, Hayato,Mashima, Kazushi
supporting information, p. 13157 - 13160 (2017/12/26)
We report a transition metal-free dehalogenation of vicinal dihalo compounds by 1,1′-bis(trimethylsilyl)-1H,1′H-4,4′-bipyridinylidene (1) under mild conditions, in which trimethylsilyl halide and 4,4′-bipyridine were generated as byproducts. The synthetic protocol for this dehalogenation reaction was effective for a wide scope of dibromo compounds as substrates while keeping the various functional groups intact. Furthermore, the reduction of vicinal dichloro alkanes and vicinal dibromo alkenes also proceeded in a salt-free manner to afford the corresponding alkenes and alkynes.
NEW ENZYMATIC PROCESS FOR THE PREPARATION OF TESTOSTERONE AND ESTERS THEREOF
-
Paragraph 0146; 0147; 0148; 0149; 0150; 0151, (2017/02/28)
The present invention relates to a new process for the preparation of testosterone by means of enzymatic hydrolysis of testosterone esters.
Method for synthesizing alkyl-acid testosterone compound
-
Paragraph 0047; 0048; 0049; 0050, (2016/10/10)
The invention provides a method for synthesizing an alkyl-acid testosterone compound. The method comprises the step of subjecting a testosterone compound to the esterification reaction with the presence of a solvent and an alkali to obtain an alkyl-acid testosterone compound. According to the technical scheme of the method for synthesizing the alkyl-acid testosterone compound, the solvent is a water-soluble organic solvent. Therefore, after the reaction, the obtained product can be precipitated through adding water, so that the overall process is simplified.
THERAPEUTIC FOR HEPATIC CANCER
-
, (2011/02/18)
A novel pharmaceutical composition for treating or preventing hepatocellular carcinoma and a method of treatment are provided. A pharmaceutical composition for treating or preventing liver cancer is obtained by combining a chemotherapeutic agent with an anti-glypican 3 antibody. Also disclosed is a pharmaceutical composition for treating or preventing liver cancer which comprises as an active ingredient an anti-glypican 3 antibody for use in combination with a chemotherapeutic agent, or which comprises as an active ingredient a chemotherapeutic agent for use in combination with an anti-glypican 3 antibody. Using the chemotherapeutic agent and the anti-glypican 3 antibody in combination yields better therapeutic effects than using the chemotherapeutic agent alone, and mitigates side effects that arise from liver cancer treatment with the chemotherapeutic agent.
Anti-Claudin 3 Monoclonal Antibody and Treatment and Diagnosis of Cancer Using the Same
-
, (2010/05/13)
Monoclonal antibodies that bind specifically to Claudin 3 expressed on cell surface are provided. The antibodies of the present invention are useful for diagnosis of cancers that have enhanced expression of Claudin 3, such as ovarian cancer, prostate cancer, breast cancer, uterine cancer, liver cancer, lung cancer, pancreatic cancer, stomach cancer, bladder cancer, and colon cancer. The present invention provides monoclonal antibodies showing cytotoxic effects against cells of these cancers. Methods for inducing cell injury in Claudin 3-expressing cells and methods for suppressing proliferation of Claudin 3-expressing cells by contacting Claudin 3-expressing cells with a Claudin 3-binding antibody are disclosed. The present application also discloses methods for diagnosis or treatment of cancers.
Use of aromatase-inhibitors for prophylaxis and/or treatment of benign prostatic hyperplasia
-
, (2008/06/13)
Aromatase-inhibitors are used in a method of prophylaxis and/or treatment by therapy of prostatic hyperplasia. Pharmaceutical preparations suitable for such a use comprise an aromatase-inhibitor. A particularly preferred aromatase-inhibitor is, for example, testolactone.
