Testosterone (Testosteronum)
Absorption of testosterone from mucous membranes and skin is high and depends on the dosage form.
It is used in the form of testosterone undecanoate (orally, intramuscularly) and active testosterone (cutaneously). About 98% of circulating testosterone is bound to SHB and albumin. Only the free fraction of testosterone is considered biologically active. Biotransformation to inactive metabolites occurs in the liver. After administration of labeled testosterone, about 90% of the radioactivity is determined in the urine in the form of glucuronide and sulfate acid conjugates. Products detected in urine include androsterone and etiocholanolone. 6% of the active substance after passing through the enterohepatic circulation is found in feces.
Testosterone, formed from testosterone undecanoate as a result of cleavage of the ester bond, is metabolized and excreted from the body in the same ways as endogenous testosterone. Undecanoic acid is metabolized by β-oxidation in the same way as other aliphatic carboxylic acids.
Features of pharmacokinetics for various routes of administration
After ingestion
a significant portion of testosterone (in the form of undecanoate ester) is absorbed in the small intestine and enters the lymphatic system, thereby partially bypassing the primary passage through the liver. From the lymphatic system, testosterone undecanoate enters the plasma. In plasma and tissues, as a result of hydrolysis, natural male sex hormones testosterone and dihydrotestosterone are released.
A single dose of 80-160 mg of testosterone undecanoate leads to a clinically significant increase in the total plasma concentration of testosterone, the maximum concentration is approximately 40 nmol/l and is achieved 4-5 hours after administration. The increased concentration of testosterone persists for at least 8 hours. The half-life is from 10 to 100 minutes.
After intramuscular injection
testosterone undecanoate is gradually released from the depot form (oil solution) and is almost completely broken down by serum esterases into testosterone and undecanoic acid. The very next day there is an increase in serum testosterone concentration.
According to two studies, in men with hypogonadism, after a single intramuscular injection of 1000 mg testosterone undecanoate, mean maximum testosterone concentrations of 45 and 24 nmol/L were determined after 7 and 14 days, respectively. Postmaximal testosterone levels decline with a half-life of approximately 53 days.
After repeated intramuscular injections of 1000 mg testosterone undecanoate into hypogonadal men with an interval of 10 weeks between injections, steady-state concentrations were achieved between the 3rd and 5th injections. The mean values of the maximum and minimum testosterone concentrations at steady state were about 42 and 17 nmol/L, respectively. Postmaximal serum testosterone levels decreased with a half-life of approximately 90 days, consistent with the rate at which the drug is released from storage.
For cutaneous application
the degree of testosterone absorption ranges from 9 to 14% of the applied dose. After absorption through the skin, testosterone enters the systemic circulation in relatively constant concentrations over a 24-hour cycle. Daily fluctuations in testosterone concentrations have the same amplitude as circadian changes in endogenous testosterone levels. External use of testosterone allows you to avoid distribution peaks in the blood that occur with the injection method of its administration. In contrast to oral androgen therapy, topical testosterone does not increase hepatic steroid concentrations above physiological norms.
The use of 50 mg of testosterone externally causes an average increase in its plasma concentration by approximately 2.5 ng/ml (8.7 nmol/l). After discontinuation of treatment, testosterone concentrations begin to decrease approximately 24 hours after the last use. The concentration returns to the original level approximately 72-96 hours after the last dose. The main active metabolites of testosterone when applied cutaneously are dihydrotestosterone and estradiol.
Testosterone norm
Men have different levels of total testosterone at the start. For some, it is initially high at a young age (10 or more ng/ml), for others it is medium (7 ng/ml), and for others it is low (4 or below ng/ml). A decrease in the initial level by 2-3 ng/ml causes certain symptoms in everyone, but the testosterone level is different.
Therefore, competent doctors, to decide on the advisability of using hormone replacement therapy, first of all pay attention to the patient’s complaints, and not to the level of total blood testosterone.
Indications
Replacement therapy for primary and secondary hypogonadism, eunuchoidism, impotence of endocrine origin, post-castration syndrome, male menopause, infertility due to impaired spermatogenesis, oligospermia, osteoporosis caused by androgen deficiency, breast cancer, menopausal disorders in women (in combination with estrogens), dysfunctional uterine bleeding due to hyperestrogenism, mastopathy, accompanied by premenstrual painful tension of the mammary glands, endometriosis, uterine fibroids.
Introduction
Wound healing is a complex process aimed at restoring the integrity of the skin and includes three phases: hemostasis/inflammation, proliferation and remodeling.
Failure of regeneration processes at any of these stages leads to disruption of the normal barrier function of the skin [1]. In this regard, the search for effective and safe substances that accelerate and normalize healing processes remains an urgent problem of modern medicine. It is known that copper is an important trace element for the normal functioning and renewal of the skin, and also plays an important role in the wound healing process, especially in the proliferation and remodeling phases [2].
I. Tenaud et al. (1999) conducted work that assessed the effect of trace elements on the expression of integrins. According to the results of the study, copper had a pronounced stimulating effect on the synthesis of integrins-a6, -b1 and -a2, located on the surface of differentiated suprabasal keratinocytes in the last phase of regeneration [3]. In a study by N. Phillips et al. (2010) showed that copper enhances the activity of matrix metalloproteinases (MMP)-1, -2 and -9, and also significantly stimulates the expression of interleukin-8, which activates collagen synthesis [4]. A.A. Rakhmetova et al. (2011) in their work assessed the wound-healing properties of ointments with copper nanoparticles in experimental animal models and came to the conclusion that these drugs statistically significantly accelerate the closure of wound defects [5].
Not all copper compounds can be used for external use. One of the methods for delivering metal ions to the skin is their complexation with various ligands, among which amino acids and peptides play a key role [6].
General Information about GHK Tripeptide
The copper-binding tripeptide GHK is a small molecule with the amino acid sequence glycyl-L-histidyl-L-lysine. It was first discovered by American researchers L. Pickart and Thaler in 1973 when comparing the effect of blood plasma of young (20–25 years) and elderly (50–70 years) people on the functioning of hepatocytes. It turned out that when exposed to the blood plasma of young people, hepatocytes begin to synthesize proteins at a level characteristic of a young organism; in particular, inhibition of fibrinogen synthesis was noted. The cause of the change in the synthetic activity of hepatocytes turned out to be GHK [7]. This discovery marked the beginning of many years of research into the properties of the tripeptide.
GHK is found naturally in blood plasma, saliva and urine. It has a high affinity for copper ion Cu2+, with which it forms the GHK-Cu chelate complex. With age, there is a significant decrease in the concentration of GHK-Cu in the blood plasma: from 200 ng/ml in children and young people to 80 ng/ml in people over 60 years of age, which may serve as one of the factors causing the reduced regenerative ability of the latter [8] .
EH Sage et al. (1994) found that GHK is released during the breakdown of the SPARC (Secreted protein acidic and rich in cysteine) protein. This glycoprotein, which is a component of the extracellular matrix, is found in large quantities in embryonic cells, as well as in tissues undergoing extensive remodeling and repair. SPARC is believed to regulate the shape and function of endothelial cells during tissue regeneration [9]. An amino acid sequence corresponding to GHK was also found in the alpha 2(I) chain of type 1 collagen. When tissue is damaged due to the action of proteases, collagen molecules are broken down and GHK is released at the site of injury [10]. Thus, GHK is a typical matrikin - a biologically active peptide released as a result of the destruction of large protein molecules of the extracellular matrix [11, 12].
The biochemical feature of the GHK tripeptide is its small size, as a result of which it penetrates cell membrane receptors better than larger molecules. In addition, GHK has unique copper-binding characteristics: the affinity of GHK for copper ions Cu2+ is much higher than that of similar peptides, and is almost equivalent to the affinity of the albumin molecule. It is assumed that GHK is involved in the transfer of copper ions from the bloodstream to tissues, and also helps them penetrate into cells in a non-toxic and easily utilized form [13]. In the works of L. Mazurowska et al. (2006, 2008) showed that the GHK-Cu complex passes well through the stratum corneum of the epidermis, and it is the tripeptide that provides adequate penetration [6, 14]. In the work of JJ Hostynek et al. (2010) obtained similar results, and also showed that when applied externally to human skin ex vivo, the GHK-Cu complex is able to accumulate in it in a concentration that is potentially effective for the treatment of inflammatory diseases not only of the skin, but also of internal organs [15].
Biological effects of GHK-Cu complex
Increased amount of collagen, glycosaminoglycans and decorin
Glycosaminoglycans, proteoglycans, collagen and fibronectin are the main components of the extracellular matrix of connective tissue. Back in 1988, FX Maquart et al. carried out work in which they showed that the GHK-Cu complex enhances collagen synthesis, and this effect is dose-dependent, with maximum stimulation at a concentration of the active substance of 10-9 M [10].
In addition to their structural function, glycosaminoglycans and proteoglycans play a role in wound healing by promoting cell adhesion, migration, and proliferation. In addition, it is believed that they can regulate the activity of growth factors. Studies by Y. Wegrowski and FX Maquart (1992, 2004) showed that the GHK-Cu complex stimulates the synthesis of not only collagen types I and III, but also dermatan sulfate [12, 16]. Later, special attention was paid to proteoglycans, especially decorin and biglucan, since they are involved in the organization of collagen fibrils. A. Simeon et al. (2000) in their study showed that the addition of GHK-Cu in vitro significantly enhanced the synthesis of collagen, glycosaminoglycans and decorin, while not affecting the synthesis of biglucan. In addition, under the influence of the complex in vivo, a change in the ratio of glycosaminoglycans towards an increase in the synthesis of chondroitin sulfate was noted [17].
T. Badenhorst et al. (2016) conducted a study on a culture of human dermal fibroblasts, which assessed the effect of the drug GHK-Cu on the synthesis of collagen, elastin and the expression of MMP-1 and MMP-2 mRNA, tissue inhibitors of metalloproteinases (TIMP)-1 and -2. On the fourth day after using GHK-Cu solutions, a significant increase in the synthesis of collagen and elastin was recorded. There was a dose-dependent reverse effect on collagen synthesis after 96 hours, with alpha-elastin synthesis increasing by approximately 30% regardless of the concentration of GHK-Cu in the drug. With increasing concentration of GHK-Cu in the preparation, the expression of MMP-1, TIMP-1 and the amount of collagen decreased [18].
Increased angiogenesis
The process of neoangiogenesis at the wound site is regulated by vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and transforming growth factor beta (TGFβ) [2]. VEGF is considered the most significant signal for stimulating angiogenesis in the wound [19]. In a study by Sen et al. (2002) assessed the effect of copper preparations on VEGF expression in human keratinocyte culture HaCaT and adult human epidermal keratinocytes. It was found that the addition of copper preparations significantly increased the expression of VEGF compared to the control group in both cell cultures. To further evaluate the potential of copper preparations in wound healing, experimental animal models (BalbC mice) were used. The results were assessed on the 5th day. Not only was there a significant decrease in the area of wounds when treated with copper preparations, but also an increase in the proliferation of epithelial tissues with an increase in cell density in the granular layer when treated with copper preparations. The authors concluded that the angiogenic potential of copper can be used to accelerate wound healing processes [20].
In the work of T. F. Lane et al. (1994), devoted to studying the properties of the SPARC protein, also assessed the effect of GHK on endothelial cells. Thus, the addition of GHK had little effect on angiogenesis. At the same time, if GHK was pretreated with a copper sulfate solution, an increase in angiogenesis was observed in strength comparable to bFGF [21].
Increased growth of nerve fibers
Often, due to an inadequate regeneration process, there is a decrease in sensitivity in the damaged area. GHK increases the production of neurotropic factors, promoting the restoration of skin innervation after damage [22].
Anti-inflammatory and antioxidant effects
SO Canapp et al. (2003) found that GHK-Cu improves ischemic wound healing and suppresses inflammation by reducing acute-phase inflammatory cytokines such as TGF-β and tumor necrosis factor alpha (TNF-α) [23].
A. Gruchlik et al. (2012) evaluated the effects of two peptides (GGH and GHK), their copper complexes and the Saccharomyces-copper enzyme on the secretion of epidermal interleukin-6 by normal human dermal fibroblasts, which plays a critical role in normal wound healing. The GHK-Cu complex has been found to reduce oxidative stress by regulating iron levels and neutralizing toxic products of lipid peroxidation. Copper-peptide complexes also reduced TNF-α-dependent secretion of interleukin-6 by fibroblasts. The authors suggest that copper-peptide drugs may in the future be used as an alternative to corticosteroid and non-steroidal anti-inflammatory drugs, which have a much wider range of side effects [24]. Later, the same authors (2014) analyzed in more detail the effect of GHK-Cu on TGF-β secretion by fibroblasts in an in vitro fibroblast culture study. It has been suggested that the copper-peptide complex has the ability to inhibit the secretion of “fibrogenic” TGF-β by fibroblasts and, as a result, regulate excessive scar formation [25].
Increasing the stem potential of cells
In YA Kang et al. (2009) studied the effect of GHK-Cu on basal keratinocytes: a significant increase in the expression of integrins, p63 protein, and proliferating cell nuclear antigen (PCNA) was detected. The results obtained indicate an increase in the proliferative potential of basal keratinocytes after the use of copper tripeptide [26]. HR Choi et al. (2012) found similar results. In addition, the researchers noted a change in the morphology of the basal cells: they acquired a more cuboid shape, which also, according to the authors, indicates an increase in the stem potential of the studied cells [27].
Bactericidal effect
Prolonged stay of neutrophils in an active state against the background of infection/contamination of wounds with various pathogens leads to the synthesis of cytolytic enzymes and oxygen free radicals, and excessive production of pro-inflammatory cytokines. The present metabolites and toxins provoke the development of tissue hypoxia, there is a decrease in the number of fibroblasts and collagen synthesis, and reepithelialization is impaired. In addition, microorganisms use nutrients and oxygen for their vital functions, which are necessary for the proper functioning of regeneration processes. Thus, maintaining aseptic conditions in the wound is an important condition for normal healing, especially in chronic wound processes [2]. In the work of I.V. Babushkina et al. (2010) showed that preparations based on copper nanoparticles have pronounced antibacterial activity against clinically significant strains of Staphylococcus aureus [28].
Normalization of wound healing and tissue regeneration processes
In studies conducted by A. Simeon et al. (1999), it was shown that the GHK-Cu complex increased the number of MMP-2 precursor molecules in wound fluid by increasing their synthesis by fibroblasts. At the same concentration, GHK-Cu stimulates the synthesis of collagen and glycosaminoglycans in cultured human fibroblasts. Thus, we can say that GHK-Cu simultaneously enhances the processes of synthesis and remodeling of the extracellular matrix. The study concluded that the GHK-Cu complex serves as a key component in stimulating the synthesis of the MMP-2 precursor. It is worth noting that during skin regeneration, MMP-2 is found in connective tissue, and MMP-9 is found in migrating keratinocytes, and the influence of these two metalloproteinases is considered critical for normal wound healing [29]. It may seem somewhat contradictory that when GHK-Cu was added to the fibroblast culture, the synthesis of MMP-2 precursors and its inhibitors, TIMP-1 and TIMP-2, simultaneously increased.
However, by forming covalent bonds with metalloproteinase molecules, TIMPs modulate their proteolytic activity, thereby regulating the process of tissue remodeling. Another property of TIMP-1 and TIMP-2 is their ability to act as a growth factor for some cells. In particular, TIMP-2 stimulates fibroblast proliferation by increasing protein kinase A activity [30].
The effect of copper tripeptide GHK-Cu on skin regeneration processes
Over the more than forty-year history of studying GHK-Cu, many studies have been carried out using experimental models that studied the effect of the complex on regeneration processes. It is worth noting that in the vast majority of studies, GHK-Cu had a pronounced positive effect on the healing process of various wound surfaces. Thus, in a study by SO Canapp et al. (2003) showed that topical application of copper tripeptide significantly accelerated the closure of wound defects in experimental rats when compared with a placebo group and with a group in which hydroxypropyl methylcellulose (medicinal base) was used [23].
IT Cangul et al. (2006) compared the effect of GHK-Cu and zinc oxide on the healing of open wounds in rabbits: it was shown that in the GHK-Cu group, full-fledged granulation tissue was formed by the 7th day, while in the zinc oxide group and in the control group it was just beginning to take shape. Also, by day 7, the wound area in the tripeptide group was significantly smaller than in the zinc oxide and control groups, but by day 21 there was no significant difference between the GHK-Cu and zinc oxide groups [31]. In the work of A.A. Kurtseva (2008) assessed the effect of the GHK tripeptide and its constituent amino acids on reparative processes in rats. The tripeptide has been found to accelerate wound healing. These results were confirmed by an increase in the relative wound healing coefficient by 1.8 times compared to the control group. The maximum effect developed by days 6–10, which was reflected by an even greater increase in the coefficient of relative wound healing – 2.7 times [32].
Use of copper tripeptide GHK-Cu in clinical practice
Clinical studies using GHK-Cu-based drugs are few and their results are inconsistent. In a prospective, randomized, blinded, placebo-controlled study, JB Bishop et al. (1992) compared the effectiveness of GHK-Cu (0.4% cream) and silver sulfadiazine (1% cream) with placebo in 86 patients with chronic venous ulcers. By the end of the 4th week, there was a significant reduction in ulcer size in patients in the silver sulfadiazine group compared with the tripeptide and placebo groups, and there were no statistically significant differences between the latter two groups [33]. However, in 1994 GD Mulder et al. conducted a randomized, multicenter, blinded, placebo-controlled study to evaluate the efficacy and safety of 2% GHK-Cu gel in the treatment of neuropathic ulcers in diabetic patients following surgical debridement. The following results were obtained: in the group of patients who used the gel with GHK-Cu, the closure of ulcerative defects occurred 3 times faster than in the group receiving standard treatment and in the placebo group. In addition, the authors noted that the incidence of infectious complications was noticeably lower in the copper tripeptide group [34].
Conclusion
The GHK-Cu complex has a wide range of biological effects, thanks to which it can be used in various fields of medicine where improvement/acceleration of regeneration processes is required, incl. for healing skin wounds. GHK-Cu has demonstrated a high safety and efficacy profile in in vitro studies and in in vivo experimental models. At the same time, today there is no convincing evidence base on the use of this substance in clinical practice, and the results of the few clinical studies available are contradictory, and therefore it seems advisable to conduct new studies to assess the real effectiveness of GHK-Cu in practical medicine.
Testosterone propionate[edit | edit code]
Yuzhakov Anton Testosterone description of the drug
Yuzhakov Anton TESTOSTERONE PROPIONATE HOW TO CORRECTLY EXIT THE PROPIONATE COURSE
Yuzhakov Anton FIRST COURSE. COMPILATION, SELECTION OF DOSES, CONTROL OF ANALYSIS.
Testosterone propionate (Ukraine) Propionate from Gerth Pharmaceuticals (volume 10ml, 100mg/ml)
Testosterone propionate
- one of the most popular steroids in bodybuilding. Testosterone propionate is intended for the development of muscle mass and strength, but due to the nature of its action, it is more often used during the drying period. It is one of the testosterone esters. Among the main modern manufacturers of propionate are BP (Balkan Pharmaceuticals), Magnus Pharmaceuticals, Swiss Remedies, Farmakom, Indian Testopin from BM Pharmaceuticals, Ukrainian Testosterone propionate from Farmak, English Verormone from Nordic, Testoger P from Gerth Pharmaceuticals and some others.
Side effects of propionate[edit | edit code]
The most common complaint is pain, irritation and redness at the injection site, which is further aggravated by the high frequency of injection. Marked increase in aggression.[14]
The side effects of testosterone propionate are due to the fact that it easily aromatizes and is converted into estrogens and dihydrotestosterone, like any other testosterone ester, at high dosages it can cause:
- Gynecomastia
- Acne
- Baldness of the scalp
- Hirsutism (body hair growth)
- Prostate enlargement (especially in older people)
- Masculinization (in women)
The drug suppresses its own production of testosterone, which is usually restored at the end of the course after 2-3 months. For long-term courses, it is necessary to administer gonadotropin 500 IU, once a week, starting from 2. As practice shows, in moderate doses it does not affect the liver, kidneys, or any other internal organs. Not recommended for use by women due to high androgenic activity.
Read more:
Side effects of steroids and how to reduce harm
Interactions
When combined with substances that are inducers of microsomal liver enzymes (barbiturates, rifampicin, carbamazepine, phenylbutazone, phenytoin), the effect of testosterone may be weakened. with severe testosterone hypogonadism, propionate can be combined with drugs that stimulate thyroid function, estrogens.
Enhances the effect of anabolic agents, vitamins, drugs containing calcium, phosphorus, and slows down the elimination of cyclosporine.
Androgens may increase glucose tolerance and reduce the need for insulin or oral antidiabetic agents in persons with diabetes.
Androgens can affect the metabolism of other drugs (an increase in plasma concentrations of oxyphenbutazone was noted). In addition, it has been reported that testosterone and its derivatives increase the activity of oral anticoagulants, which may require dose adjustment. Regardless of this fact, you should always adhere to the restrictions regarding IM injections in patients with acquired or hereditary bleeding disorders.
Concomitant use of Testosterone and ACTH or corticosteroids may increase the risk of edema.
Barbiturates and alcohol reduce testosterone activity.
special instructions
Like all oil solutions, testosterone propionate is administered intramuscularly. Care must be taken to ensure that the substance being injected does not enter the vessel. with a very slow introduction of the solution, you can avoid the appearance of short-term reactions that are sometimes observed during or immediately after the injection of the oil solution (the urge to cough, coughing attacks, respiratory depression).
Prescribe with caution to patients with heart failure, hypertension, epilepsy, migraine, and impaired renal function.
In patients with a history of impaired cardiac, renal, or hepatic function, the use of androgens may cause the complication of edema with or without congestive heart failure. Caution should be exercised when using the drug in patients with conditions that cause fluid retention and cause the development of edema. Use the drug with caution in patients with porphyria.
During treatment with the drug, liver and kidney function, thyroid function, and blood glucose levels should be monitored.
Before starting treatment in men, it is necessary to exclude prostate cancer, since when using the drug androgens increase the risk of developing prostatic hyperplasia. For preventive purposes, it is recommended to conduct regular examinations of the prostate gland.
In patients taking androgens for a long period, in addition to laboratory measurements of testosterone concentrations, the following laboratory parameters should be checked: hemoglobin level, hematocrit (initially every 3 months, then once a year) and liver function tests.
Due to a possible tendency to blood clots, the drug should be prescribed with caution to men after recent surgery or injury.
Drug abuse or addiction. Androgens should not be used to enhance muscle development in healthy individuals or to enhance physical performance.
Use during pregnancy or breastfeeding. There is insufficient data on the use of the drug during pregnancy or breastfeeding. Taking into account the characteristic virilizing effect of the drug on the fetus, its use is contraindicated during pregnancy or breastfeeding. The use of the drug should be discontinued if pregnancy is diagnosed.
Children. The safety and effectiveness of use in children have not been studied, so the drug is not recommended for use in pediatric practice. The use of testosterone in children along with masculinization can cause accelerated growth and maturation of bone tissue, as well as premature closure of the epiphysis growth plate, which will result in a decrease in final growth.
The ability to influence reaction speed when driving vehicles or working with other mechanisms. While taking the drug, you should refrain from driving vehicles and operating other mechanisms.
Course design[edit | edit code]
It can be the only steroid in a “cycle”, but the best effect is achieved when combined with other drugs. Athletes starting to use anabolic drugs can recommend dosages of 50 mg of propionate every other day. The usual dose for more experienced athletes is 100 mg propionate daily and above.
Be sure to take anti-estrogenic drugs, such as Proviron or aromatase inhibitors, according to the standard regimen, starting from the second week to avoid the development of gynecomastia, fluid retention and other estrogenic effects. After completion of the administration, post-cycle therapy is carried out, most often tamoxifen is used. It is also advisable to take cortisol blockers at the end to maintain the gained weight. Be sure to follow a weight gain diet and take sports nutrition.
Combined course[edit | edit code]
When drying, it combines well with stanozolol, trenbolone acetate, Masteron, Primobolan and some other drugs. Propionate is included in mixtures of testosterone esters such as sustanon or omnadren, as an essential component that allows you to immediately feel the work of the steroid.
An example of a cycle for beginner “chemists” for propionate-based drying:
- Propionate 50 mg every other day
- Winstrol 30 mg per day, starting with 10 mg, and increasing the dose to the optimal dose over 1 week.
- After 6 weeks, anabolic agents should be discontinued and PCT should be started 3-4 days later.
This course demonstrates the synergistic effect of the drugs, meaning that the total effect of their simultaneous use is greater than the simple sum of the effects if they were used each separately. Some experienced athletes use local injections of propionate into the target muscle, such as the biceps, deltoids, and calves when working on mass, but this approach has not been proven to be effective.
Any form of steroid has only a resorptive effect, with no local effect on the muscle. If the drugs, when administered intramuscularly, stimulated local hypertrophy of these muscle cells, then asymmetrical growth could be observed, outwardly similar to the results obtained with the use of synthol.
Note!
Description of the drug Testosterone propionate solution d/in. 5% amp. 1ml No. 5 on this page is a simplified author’s version of the apteka911 website, created on the basis of the instructions for use.
Before purchasing or using the drug, you should consult your doctor and read the manufacturer's original instructions (attached to each package of the drug). Information about the drug is provided for informational purposes only and should not be used as a guide to self-medication. Only a doctor can decide to prescribe the drug, as well as determine the dose and methods of its use.
