Progesterone CAS 57-83-0 Legal Steroids
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|Min. Order:||10 g|
|Min. Order||FOB Price|
|10 g||US $10/ g|
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- Model NO.: 57-83-0
- Customized: Non-Customized
- Suitable for: Elderly, Children, Adult
- Purity: >99%
- Transport Package: 1kg Sterile Aluminum Foil Bag or Discreet
- Origin: China
- Powder: Yes
- Certification: GMP, ISO 9001, USP, BP
- State: Solid
- Trademark: LSW
- Specification: 1kg/bag
- HS Code: 3006920000
Progesterone (abbreviated as P4), also known as pregn-4-ene-3,20-dione, is an endogenous steroid and progestogen sex hormone involved in the menstrual cycle, pregnancy, and embryogenesis of humans and other species. It belongs to a group of steroid hormones called the progestogens, and is the major progestogen in the body. Progesterone is also a crucial metabolic intermediate in the production of other endogenous steroids, including the sex hormones and the corticosteroids, and plays an important role in brain function as a neurosteroid.
It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system.
Progesterone is the most important progestogen in the body, the result of its action as a potent agonist of the nuclear progesterone receptor (nPR) (with an affinity of KD = 1 nM). In addition, progesterone is an agonist of the more recently discovered membrane progesterone receptors (mPRs), as well as a ligand of the PGRMC1 (progesterone receptor membrane component 1; formerly known as the σ2 receptor). Moreover, progesterone is also known to be an antagonist of the σ1 receptor, a negative allosteric modulator of the nACh receptors, and a potent antagonist of the mineralocorticoid receptor (MR). Progesterone prevents MR activation by binding to this receptor with an affinity exceeding even those of aldosterone and glucocorticoids such as cortisol and corticosterone, and produces antimineralocorticoid effects, such as natriuresis, at physiological concentrations. In addition, progesterone binds to and behaves as a partial agonist of the glucocorticoid receptor (GR), albeit with very low potency (EC50 >100-fold less relative to cortisol).
Progesterone, through its neurosteroid active metabolites such as 5α-dihydroprogesterone and allopregnanolone, acts indirectly as a positive allosteric modulator of the GABAA receptor.
Progesterone and some of its metabolites, such as 5β-dihydroprogesterone, are agonists of the pregnane X receptor (PXR), albeit weakly so (EC50 >10 µM). In accordance, progesterone induces several hepatic cytochrome P450 enzymes, such as CYP3A4, especially during pregnancy when concentrations are much higher than usual. Premenopausal women have been found to have greater CYP3A4 activity relative to men and postmenopausal women, and it has been inferred that this may be due to the higher progesterone levels present in premenopausal women.
Progesterone modulates the activity of CatSper (cation channels of sperm) voltage-gated Ca2+ channels. Since eggs release progesterone, sperm may use progesterone as a homing signal to swim toward eggs (chemotaxis). As a result, it has been suggested that substances that block the progesterone binding site on CatSper channels could potentially be used in male contraception.
Progesterone binds extensively to plasma proteins, including albumin (50-54%) and transcortin (43-48%). It has similar affinity for albumin relative to the PR.
Interactions with other steroid hormones
Progesterone has a number of physiological effects that are amplified in the presence of estrogens. Estrogens through estrogen receptors (ERs) induce or upregulate the expression of the PR. One example of this is in breast tissue, where estrogens allow progesterone to mediate lobuloalveolar development.
Elevated levels of progesterone potently reduce the sodium-retaining activity of aldosterone, resulting in natriuresis and a reduction in extracellular fluid volume. Progesterone withdrawal, on the other hand, is associated with a temporary increase in sodium retention (reduced natriuresis, with an increase in extracellular fluid volume) due to the compensatory increase in aldosterone production, which combats the blockade of the mineralocorticoid receptor by the previously elevated level of progesterone.
Progesterone has key effects via non-genomic signalling on human sperm as they migrate through the female tract before fertilization occurs, though the receptor(s) as yet remain unidentified. Detailed characterisation of the events occurring in sperm in response to progesterone has elucidated certain events including intracellular calcium transients and maintained changes, slow calcium oscillations, now thought to possibly regulate motility. It is produced by the ovaries. Interestingly, progesterone has also been shown to demonstrate effects on octopus spermatozoa.
Progesterone is sometimes called the "hormone of pregnancy", and it has many roles relating to the development of the fetus:
- Progesterone converts the endometrium to its secretory stage to prepare the uterus for implantation. At the same time progesterone affects the vaginal epithelium and cervical mucus, making it thick and impenetrable to sperm. Progesterone is anti-mitogenic in endometrial epithelial cells, and as such, mitigates the tropic effects of estrogen. If pregnancy does not occur, progesterone levels will decrease, leading, in the human, to menstruation. Normal menstrual bleeding is progesterone-withdrawal bleeding. If ovulation does not occur and the corpus luteum does not develop, levels of progesterone may be low, leading to anovulatory dysfunctional uterine bleeding.
- During implantation and gestation, progesterone appears to decrease the maternal immune response to allow for the acceptance of the pregnancy.
- Progesterone decreases contractility of the uterine smooth muscle.
- In addition progesterone inhibits lactation during pregnancy. The fall in progesterone levels following delivery is one of the triggers for milk production.
- A drop in progesterone levels is possibly one step that facilitates the onset of labor.
The fetus metabolizes placental progesterone in the production of adrenal steroids.
Progesterone plays an important role in mammary gland development in females. In conjunction with prolactin, it mediates lobuloalveolar maturation of the breasts during pregnancy to allow for milk production, and thus lactation and breastfeeding after childbirth. Estrogen is required for progesterone to mediate lobuloalveolar maturation, as it induces expression of the PR in breast tissue. Moreover, it has been found that RANKL is a critical downstream mediator of progesterone-mediated lobuloalveolar development. Knockout mice of RANKL show an almost identical mammary phenotype relative to PR knockout mice, including normal mammary ductal development but complete failure of the development of lobuloalveolar structures.
Though to a far lesser extent than estrogen, which is the major mediator of breast ductal development (via ERα, specifically), progesterone has been found to be involved in ductal development as well. PR knockout mice or mice treated with the PR antagonist mifepristone show delayed but otherwise normal ductal development at puberty. In addition, mice modified to have overexpression of PRA display ductal hyperplasia, and progesterone induces ductal growth in mouse mammary gland. Progesterone mediates ductal development mainly via the induction of amphiregulin, the same growth factor that estrogen primarily induces to mediate ductal development. These findings suggest that, while not essential for full ductal development, progesterone seems to play a potentiating or accelerating role in estrogen-mediated ductal development, at least in mice.
Progesterone also appears to be involved in the pathophysiology of breast cancer, though its role, and whether it is a promoter or inhibitor of breast cancer risk, has not been fully elucidated. In any case, while certain synthetic progestins with androgenic effects such as medroxyprogesterone acetate and 19-nortestosterone derivatives including norethisterone acetate, norgestrel, and levonorgestrel have been found to significantly increase the risk of breast cancer in postmenopausal women in combination with estrogen as a component of hormone replacement therapy, the combination of natural progesterone or the pure, non-androgenic progestin dydrogesterone with estrogen has been found not to do so. In fact, progesterone or dydrogesterone added to estrogen appear to decrease the risk of breast cancer relative to estrogen alone.
Progesterone and its neurosteroid active metabolite allopregnanolone appear to be importantly involved in sex drive in females.
Dr. Diana Fleischman, of the University of Portsmouth, and colleagues examined the relationship between progesterone and sexual attitudes. Their research was published in the Archives of Sexual Behavior. They found that women who have higher levels of progesterone are more likely to be open to the idea of engaging in sexual behaviour with other women. Similarly, when heterosexual men are subtly reminded of the importance of having male friends and allies, they report more positive attitudes toward engaging in sexual behaviour with other men. This pattern is particularly dramatic in men who have high levels of progesterone.
Progesterone, like pregnenolone and dehydroepiandrosterone (DHEA), belongs to an important group of endogenous steroids called neurosteroids. It can be synthesized within the central nervous system and also serves as a precursor to another major neurosteroid, allopregnanolone.
Neurosteroids are neuromodulators, and are neuroprotective, neurogenic, and regulate neurotransmission and myelination. The effects of progesterone as a neurosteroid are mediated predominantly through its interactions with non-nuclear PRs, namely the mPRs and PGRMC1, as well as certain other receptors, such as the σ1 and nACh receptors.
Since most progesterone in males is created during testicular production of testosterone, and most in females by the ovaries, the shutting down (whether by natural or chemical means), or removal, of those inevitably causes a considerable reduction in progesterone levels. Previous concentration upon the role of progestogens in female reproduction, when progesterone was simply considered a "female hormone", obscured the significance of progesterone elsewhere in both sexes.
The tendency for progesterone to have a regulatory effect, the presence of progesterone receptors in many types of body tissue, and the pattern of deterioration (or tumor formation) in many of those increasing in later years when progesterone levels have dropped, is prompting widespread research into the potential value of maintaining progesterone levels in both males and females.
Studies as far back as 1987 show that female sex hormones have an effect on the recovery of traumatic brain injury. In these studies, it was first observed that pseudopregnant female rats had reduced edema after traumatic brain injury. Recent clinical trials have shown that among patients that have suffered moderate traumatic brain injury, those that have been treated with progesterone are more likely to have a better outcome than those who have not.
Previous studies have shown that progesterone supports the normal development of neurons in the brain, and that the hormone has a protective effect on damaged brain tissue. It has been observed in animal models that females have reduced susceptibility to traumatic brain injury and this protective effect has been hypothesized to be caused by increased circulating levels of estrogen and progesterone in females. A number of additional animal studies have confirmed that progesterone has neuroprotective effects when administered shortly after traumatic brain injury. Encouraging results have also been reported in human clinical trials.
The mechanism of progesterone protective effects may be the reduction of inflammation that follows brain trauma.
Damage incurred by traumatic brain injury is believed to be caused in part by mass depolarization leading to excitotoxicity. One way in which progesterone helps to alleviate some of this excitotoxicity is by blocking the voltage-dependent calcium channels that trigger neurotransmitter release. It does so by manipulating the signaling pathways of transcription factors involved in this release. Another method for reducing the excitotoxicity is by up-regulating the GABAA, a widespread inhibitory neurotransmitter receptor.
Progesterone has also been shown to prevent apoptosis in neurons, a common consequence of brain injury. It does so by inhibiting enzymes involved in the apoptosis pathway specifically concerning the mitochondria, such as activated caspase 3 and cytochrome c.
Not only does progesterone help prevent further damage, it has also been shown to aid in neuroregeneration. One of the serious effects of traumatic brain injury includes edema. Animal studies show that progesterone treatment leads to a decrease in edema levels by increasing the concentration of macrophages and microglia sent to the injured tissue. This was observed in the form of reduced leakage from the blood brain barrier in secondary recovery in progesterone treated rats. In addition, progesterone was observed to have antioxidant properties, reducing the concentration of oxygen free radicals faster than without. There is also evidence that the addition of progesterone can also help remyelinate damaged axons due to trauma, restoring some lost neural signal conduction. Another way progesterone aids in regeneration includes increasing the circulation of endothelial progenitor cells in the brain. This helps new vasculature to grow around scar tissue which helps repair the area of insult.
Vitamin D and progesterone separately have neuroprotective effects after traumatic brain injury, but when combined their effects are synergistic. When used at their optimal respective concentrations, the two combined have been shown to reduce cell death more than when alone.
One study looks at a combination of progesterone with estrogen. Both progesterone and estrogen are known to have antioxidant-like qualities and are shown to reduce edema without injuring the blood-brain barrier. In this study, when the two hormones are administered alone it does reduce edema, but the combination of the two increases the water content, thereby increasing edema.
The clinical trials for progesterone as a treatment for traumatic brain injury have only recently begun. ProTECT, a phase II trial conducted in Atlanta at Grady Memorial Hospital in 2007, the first to show that progesterone reduces edema in humans. Since then, trials have moved on to phase III. The National Institute of Health began conducting a nationwide phase III trial in 2011 led by Emory University. A global phase III initiative called SyNAPSe®, initiated in June 2010, is run by a U.S.-based private pharmaceutical company, BHR Pharma, and is being conducted in the United States, Argentina, Europe, Israel and Asia. Approximately 1,200 patients with severe (Glasgow Coma Scale scores of 3-8), closed-head TBI will be enrolled in the study at nearly 150 medical centers.
Progesterone enhances the function of serotonin receptors in the brain, so an excess or deficit of progesterone has the potential to result in significant neurochemical issues. This provides an explanation for why some people resort to substances that enhance serotonin activity such as nicotine, alcohol, and cannabis when their progesterone levels fall below optimal levels.
- To examine the effects of progesterone on nicotine addiction, participants in one study were either treated orally with a progesterone treatment, or treated with a placebo. When treated with progesterone, participants exhibited enhanced suppression of smoking urges, reported higher ratings of "bad effects" from IV nicotine, and reported lower ratings of "drug liking". These results suggest that progesterone not only alters the subjective effects of nicotine, but reduces the urge to smoke cigarettes.
- Sex differences in hormone levels may induce women to respond differently than men to nicotine. When women undergo cyclic changes or different hormonal transition phases (menopause, pregnancy, adolescence), there are changes in their progesterone levels. Therefore, females have an increased biological vulnerability to nicotine's reinforcing effects compared to males and progesterone may be used to counter this enhanced vulnerability. This information supports the idea that progesterone can affect behavior.
- Similar to nicotine, cocaine also increases the release of dopamine in the brain. The neurotransmitter is involved in the reward center and is one of the main neurotransmitters involved with substance abuse and reliance. In a study of cocaine users, it was reported that progesterone reduced craving and the feeling of being stimulated by cocaine. Thus, progesterone was suggested as an agent that decreases cocaine craving by reducing the dopaminergic properties of the drug.
- During pregnancy, progesterone is said to decrease irritability.
- During pregnancy, progesterone helps to suppress immune responses of the mother to fetal antigens, which prevents rejection of the fetus.
- Progesterone raises epidermal growth factor-1 (EGF-1) levels, a factor often used to induce proliferation, and used to sustain cultures, of stem cells.
- Progesterone increases core temperature (thermogenic function) during ovulation.
- Progesterone reduces spasm and relaxes smooth muscle. Bronchi are widened and mucus regulated. (PRs are widely present in submucosal tissue.)
- Progesterone acts as an antiinflammatory agent and regulates the immune response.
- Progesterone reduces gall-bladder activity.
- Progesterone normalizes blood clotting and vascular tone, zinc and copper levels, cell oxygen levels, and use of fat stores for energy.
- Progesterone may affect gum health, increasing risk of gingivitis (gum inflammation).
- Progesterone appears to prevent endometrial cancer (involving the uterine lining) by regulating the effects of estrogen.
- Progesterone plays an important role in the signaling of insulin release and pancreatic function, and may affect the susceptibility to diabetes or gestational diabetes.
- Progesterone may play a role in male behavior, such as in male aggression towards infants.
The use of progesterone and its analogues have many medical applications, both to address acute situations and to address the long-term decline of natural progesterone levels. Because of the poor bioavailability of progesterone when taken orally, many synthetic progestins have been designed with improved oral bioavailability and have been used long before progesterone formulations became available. Progesterone was approved by the United States Food and Drug Administration as vaginal gel on July 31, 1997, an oral capsule on May 14, 1998 in an injection form on April 25, 2001 and as a vaginal insert on June 21, 2007. Progesterone is marketed under a large number of different brand names throughout the world.
Progesterone, when taken orally, has very poor pharmacokinetics, including low bioavailability (only about 10-15% reaches the bloodstream) and a half-life of only about 5 minutes, unless it is micronized. As such, it is sold in the form of oil-filled capsules containing micronized progesterone for oral use (Utrogestan, Prometrium, Microgest), termed oral micronized progesterone (OMP). Progesterone is also available in the forms of vaginal or rectal suppositories or pessaries (Cyclogest), transdermally-administered gels or creams (Crinone, Endometrin, Progestogel, Prochieve), or via intramuscular or subcutaneous injection of a vegetable oil solution (Progesterone, Strone).
Transdermal products made with progesterone USP (i.e., "natural progesterone") do not require a prescription. Some of these products also contain "wild yam extract" derived from Dioscorea villosa, but there is no evidence that the human body can convert its active ingredient (diosgenin, the plant steroid that is chemically converted to produce progesterone industrially) into progesterone.
The route of administration impacts the effects of progesterone. OMP has a wide inter-individual variability in absorption and bioavailability. In contrast, progestins are rapidly absorbed with a longer half-life than progesterone and maintain stable levels in the blood. The absorption and bioavailability of OMP is increased approximately two-fold when it is taken with food.
Progesterone has a relatively short half-life in the body. As such, OMP is usually prescribed for twice or thrice-daily administration or once-daily administration when taken by injection. Via the oral route, peak concentrations are seen about 2-3 hours after ingestion, and the half-life is about 16-18 hours. Significantly elevated serum levels of progesterone are maintained for about 12 hours, and levels do not return to baseline until at least 24 hours have passed.
OMP is prescribed in divided doses of 25-400 mg/daily, but in the range of 100-300 mg per day most commonly. Oral doses of 100-200 mg will result in serum progesterone levels greater than 10 ng/mL. Notably, a portion of progesterone is converted into 5α-dihydroprogesterone and allopregnanolone (a conversion that is catalyzed by the enzymes 5α-reductase and 3α-hydroxysteroid dehydrogenase (3α-HSD) and occurs in the liver, reproductive endocrine tissues, skin, and the brain), which are neurosteroids and potent potentiators of GABAA receptors. It is for this reason that common reported side effects of progesterone include dizziness, drowsiness or sedation, sleepiness, and fatigue, especially at high doses. As a result, some physicians may instruct their patients to take their progesterone before bed. Both oral and intramuscularly injected progesterone produce sedative effects, indicating that first-pass metabolism in the liver is not essential for the conversion to take place. Moreover, the sedative effects occur in both men and women, indicating a lack of sex-specificity of the effects.
There are several notable drug interactions with progesterone. Selective serotonin reuptake inhibitors (SSRIs) may increase the GABAA receptor-related central depressant effects of progesterone by enhancing its conversion into 5α-dihydroprogesterone and allopregnanolone via activation of 3α-HSD. Progesterone potentiates the sedative effects of benzodiazepines and ethanol. Notably, there is a case report of progesterone abuse alone with very high doses. 5α-Reductase inhibitors such as finasteride and dutasteride, as well as inhibitors of 3α-HSD such as medroxyprogesterone acetate, inhibit the conversion of progesterone into its inhibitory neurosteroid metabolites, and for this reason, may have the potential to block or reduce its sedative effects.
Progesterone is a weak but significant agonist of the PXR, and has been found to induce several hepatic cytochrome P450 enzymes, such as CYP3A4, especially when concentrations are high, such as with pregnancy range levels. As such, progesterone may have the potential to accelerate the clearance of various drugs, especially with oral administration (which results in supraphysiological levels of progesterone in the liver), as well as with the high concentrations achieved with sufficient injection dosages.
Progesterone, when taken orally, undergoes gastrointestinal (especially hepatic) metabolism to form hydroxylated metabolites, which in turn are metabolized into sulfate and glucuronide derivatives. Enzymes involved in the hepatic metabolism of progesterone include, particularly, CYP2C19 and CYP3A4, as well as CYP2C9.
Transdermal progesterone is about 5-7 times stronger than oral progesterone. This is due to the fact transdermal administration bypasses first-pass metabolism. As such, 20-30 mg/day transdermal progesterone is equivalent to about 100-200 mg/day oral progesterone.
With vaginal and rectal administration, a 100 mg dose of progesterone results in peak levels at 4 hours and 8 hours after dosing, respectively, with the levels achieved being in the serum luteal phase range. Following peak serum concentrations, there is a gradual decline in plasma levels, and after 24 hours, serum levels typical of the follicular phase are reached.
With intramuscular injection of 10 mg progesterone suspended in vegetable oil, maximum plasma concentrations (Cmax) are reached at approximately 8 hours after administration, and serum levels remain above baseline for about 24 hours. Doses of 10 mg, 25 mg, and 50 mg via intramuscular injection result in mean maximum serum concentrations of 7 ng/mL, 28 ng/mL, and 50 ng/mL, respectively. With intramuscular injection, a dose of 25 mg results in normal luteal phase serum levels of progesterone within 8 hours, and a 100 mg dose produces mid-pregnancy levels. At these doses, serum levels of progesterone remain elevated above baseline for at least 48 hours.
Due to the high concentrations achieved, progesterone by intramuscular injection at the usual clinical dose range is able to suppress gonadotropin secretion from the pituitary gland, demonstrating antigonadotropic efficacy.
Progesterone can also be administered alternatively via subcutaneous injection, with the aqueous new formulation Prolutex being intended specifically for once-daily administration by this route. This formulation is rapidly absorbed and has been found to result in higher serum peak progesterone levels relative to intramuscular oil formulations. In addition, subcutaneous injection of progesterone is considered to be easier, safer (less risk of injection site reactions), and less painful relative to intramuscular injection.
For comparative purposes, mid-luteal serum levels of progesterone are above 5-9 ng/ml, plasma levels in the first 4 to 8 weeks of pregnancy are 25-75 ng/ml, and serum levels at term are typically around 200 ng/ml. Production of progesterone in late pregnancy is approximately 250 mg per day, 90% of which reaches maternal circulation.
Prevention of preterm birth
Vaginally dosed progesterone is being investigated as potentially beneficial in preventing preterm birth in women at risk for preterm birth. The initial study by Fonseca suggested that vaginal progesterone could prevent preterm birth in women with a history of preterm birth. According to a recent study, women with a short cervix that received hormonal treatment with a progesterone gel had their risk of prematurely giving birth reduced. The hormone treatment was administered vaginally every day during the second half of a pregnancy. A subsequent and larger study showed that vaginal progesterone was no better than placebo in preventing recurrent preterm birth in women with a history of a previous preterm birth, but a planned secondary analysis of the data in this trial showed that women with a short cervix at baseline in the trial had benefit in two ways: a reduction in births less than 32 weeks and a reduction in both the frequency and the time their babies were in intensive care. In another trial, vaginal progesterone was shown to be better than placebo in reducing preterm birth prior to 34 weeks in women with an extremely short cervix at baseline. An editorial by Roberto Romero discusses the role of sonographic cervical length in identifying patients who may benefit from progesterone treatment. A meta-analysis published in 2011 found that vaginal progesterone cut the risk of premature births by 42 percent in women with short cervixes. The meta-analysis, which pooled published results of five large clinical trials, also found that the treatment cut the rate of breathing problems and reduced the need for placing a baby on a ventilator.
- Progesterone is used for luteal support in Assisted Reproductive Technology (ART) cycles such as In-vitro Fertilization (IVF).
- Progesterone is used to control persistent anovulatory bleeding. It is also used to prepare uterine lining in infertility therapy and to support early pregnancy. Patients with recurrent pregnancy loss due to inadequate progesterone production may receive progesterone.
- Progesterone is also used in nonpregnant women with a delayed menstruation of one or more weeks, in order to allow the thickened endometrial lining to slough off. This process is termed a progesterone withdrawal bleed. The progesterone is taken orally for a short time (usually one week), after which the progesterone is discontinued and bleeding should occur.
- Progesterone can be used to treat catamenial epilepsy by supplementation during certain periods of the menstrual cycle.
- Progesterone is being investigated as potentially beneficial in treating multiple sclerosis, since the characteristic deterioration of nerve myelin insulation halts during pregnancy, when progesterone levels are raised; deterioration commences again when the levels drop.
- Progesterone also has a role in skin elasticity and bone strength, in respiration, in nerve tissue and in female sexuality, and the presence of progesterone receptors in certain muscle and fat tissue may hint at a role in sexually dimorphic proportions of those.[copyright violation?]
- Antiprogestins and selective progesterone receptor modulators (SPRM)s, such as mifepristone, can be used to prevent conception or induce medical abortions (note that methods of hormonal contraception do not contain progesterone but a progestin).
- Progesterone is starting to be used in the treatment of the skin condition hidradenitis suppurativa.
- Progesterone is sometimes employed as a component of hormone replacement therapy for trans women.
Progesterone was independently discovered by four research groups.
Willard Myron Allen co-discovered progesterone with his anatomy professor George Washington Corner at the University of Rochester Medical School in 1933. Allen first determined its melting point, molecular weight, and partial molecular structure. He also gave it the name Progesterone derived from Progestational Steroidal ketone. The drug was originally administered by injection because it rapidly inactivated after oral use 
- When you supplement with Nandrolone-Decanoate, as is with all anabolic steroids, your natural testosterone production will be suppressed; in this case it will be completely suppressed from one single dosing. A single 100mg injection of Nandrolone-Decanoate is all it takes to suppress all testosteron production. For this reason, it is imperative that you supplement with some form of exogenous testosteron when you supplement with the Nandrolon compound. Failure to do so will result in a low testosteron condition, and this is simply not good for your health. Further, testosterone is a fantastic, highly versatile and generally well-tolerated anabolic steroid your body is very familiar with and will only enhance your total results.
- Nandrolon-Decanoate does aromatize to a degree; approximately 20% the rate of testosterone. Further, this is a steroid that carries a progestin nature and by these traits can lead to Gynecomastia. With the use of an Aromatase Inhibitor, Gynecomastia can be avoided; Arimidex and Letrozole will both do the trick. Further, an Aromatase Inhibitor will aid in combating water retention that can occur with this steroid.
- When supplementing with Nandrolon-Decanoate, 8 weeks of total use should be the minimal time frame of use. Any use less than 8 weeks will provide very little as this is such a slow acting steroid, and will simply be a waste of time. To maximize your results, 10-12 weeks of total use will be far more optimal, with 16 weeks generally being the maximal time frame of use.
- Whenever you decide to discontinue anabolic steroid use, you do not want to end use while still supplementing with Nandrolon-Decanoate. As a steroid with a very long activity time, if you end use with a large amount still freshly in your system it can make recovery a tremendously difficult process. In most cases, all Nandrolone-Decanoate use should end at least 2 weeks before all anabolic steroid use comes to a halt; many will find 4 weeks to be needed.
Nandrolon Decanoate Dosage Recommendations for Bodybuilding Cycles
Numerous individuals may find it really difficult to come up with the proper Nandrolone Decanoate dosage to take in their cycle. There is limited information online that gives accurate advice and many of the articles suggest lower doses than what should be used. Uses often decide to overcompensate with testosterone and shortchange their Deca doses due to the fact that the hormone is so suppressive to natural testosterone production. In order to achieve positive results, you will need to keep total hormonal balance. To avoid any problems, you have to keep your estrogen levels in normal limits and offer the body the necessary quantity of testosterone.
Numerous individuals are unaware of the possible results of using some particular Nandrolone Decanoate doses. Many bodybuilders use this steroid in the off-season bulking cycles so as to promote muscle size and growth. In case bulking is not the main target of the bodybuilder, lower Nandrolone Decanoate doses can be really beneficial.
TABLE OF CONTENTS: Deca Durabolin | Nandrolon Decanoate | Nandrolon Phenylpropionate | Cycle Schedules | Deca Test Cycle | Dosage Guidelines | Before & After Results | Reported Gains| Side Effects | Deca Durabolin for Sale | USA & Canada | United Kingdom | Deca 200 | Deca Durabolin 300
Off-season Nandrolon Decanoate Doses:
It is enough to take 300-400mg of Nandrolon Decanoate per week in the off-season. For this, you will need to take one injection each week. To increase the efficiency of the steroid, the majority of bodybuilders will split the injection into 2 small equal size injections per week. This task will reduce the total injection volume. You can increase your dosage in case you tolerate 300-400mg without any problems. Even though there is no need for high dosages, we need to know that most men will support 60mg per week without any major problems. It is enough to stick with 400mg. It is more likely to experience negative side effects in case you increase the dosage. In some cases, the negative effects may outweigh the positive effects, even though this may differ from one person to another.
Dosages for Cutting Before a Contest
The Nandrolon hormone may be identified in numerous competitive bodybuilding contest cycles, even though the majority of bodybuilders don`t consider Nandrolon Decanoate to be a cutting steroid. People may find this steroid to be really useful, even though it does not offer the conditioning effects of Trenbolone, Anavar or Winstrol. People may obtain numerous benefits by taking 200-300mg Nandrolon Decanoate doses on a weekly basis. Even though this steroid has a powerful ability in preserving lean tissue, there is another benefit that is far more important.
During the demanding cutting cycle of the bodybuilding domain, the body needs a lot of relief, which can be provided by a low Nandrolone Decanoate doses. The hard dieting combined with hard training session can really tire the body. Apart from offering a powerful therapeutic relief, low Nandrolon Decanoate doses will also improve muscular endurance throughout the demanding training sessions.
Other Uses of Nandrolon Decanoate Cycles
Numerous individuals don`t view Nandrolon Decanoate as adequate for improving athletic performance due to the fact that it is primarily regarded as a bulking steroid. Many athletes prefer these steroid due to the fact that they understand it`s potential. It will not be any problem in case the athlete does not need to grow. You will never grow in case you do not consume high quantity of calories and take important Nandrolon Decanoate doses. The individual will take the Deca Dorabolin doses simply to obtain a therapeutic relief in this situation. This is the main goal, even though the steroid also improves the muscular endurance. It will be enough to consume 100-200mg of Nandrolon Decanoate on a weekly basis. To obtain the true benefits, you need to stick with the 200mg dose. View the best Deca Durabolin stacks and cycle dosages here.
How Long Should your Cycle Be?
After you have selected your dosage for Nandrolon Decanoate, the next step will be to establish the entire time frame of usage. Considering the important Decanoate ester attached to the steroid, we can state that Nandrolon Decanoate acts really slowly. Therefore, this is not recommended for short term usage. You will have to use the steroid for a minimum of 8 weeks in order to reap the benefits, regardless of the doses that you select. However, most men will usually take the steroid for 10-12 weeks. This is the perfect time frame, even though some may go up to 16 weeks.
Sexual Side Effects from Nandrolone Use
Nandrolon Decanoate Dosage CycleIn case you encounter any sexually related side effects, such as erectile dysfunction or los of libido, you often make improper adjustments. Most individuals will likely presume the fact that their testosteron dose has dropped below normal levels. These individuals will usually increase the testosteron level, regardless if their Nandrolon Decanoate doses are at the low end range. While this may work in some cases, the problem will get worst in most of the situations.
You may consider the fact that your hormone levels are unbalanced in case you have experiencing some problems. You are simply aggravating the problem in case you add more testosteron. You can experience sexually related side effects in case you don`t manage to control your estrogen levels. Your estrogen levels should be neither too high nor too low in order to avoid any sexually related issues.
However, what is the perfect way to solve this issue? You just need to make sure you have sufficient testosterone in your body. The next step will be to maintain a normal estrogen level in your body. You will definitely avoid all side effects if you manage to respect these two aspects. Click here to find Deca Durabolin for Sale.
Nandrolon Decanoate, Dianabol and Testosteron Cycle
In case you replace the testosteron, Nandrolon Decanoate and Dbol cycle with sustanon, this cycle can be used without the help of a test.
Week Testosteron Cypionate Deca Durabolin Dianabol Ostarine MK-2866 Aromasin N2Guard
1 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
2 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
3 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
4 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
5 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
6 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
7 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
8 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
9 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
10 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
11 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
12 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
The half-life of Nandrolone Decanoate Nearly six days, however it requires about 21 days to become released out of your organism. Actually, several sportsmen have positive for the metabolite months following their final injection, therefore always be cautious with your Nandrolone decanoate dosage per week and give yourself lots of time before a potential test might occur.
Quick Detail :
Nandrolon Decanoate / Nandro Deca / DECA / Durabolin
Nandrolon Decanoate Chemical Name: 4-estren-17beta-ol-3-one decanoate
Durabolin Synonyms: 19-nortestosterone 17-decanoate; 19-nortestoterone decanoate
DECA Molecular Formula: C28H44O3
Nandrolone Decanoate Molecular weight: 428.65
Durabolin CAS NO.: 360-70-3
DECA EINECS: 206-639-3
DECA Assay: 99% min.
Nandrolon Decanoate Appearance: white or oyster white to pale yellow crystalline powder
Durabolin Usage: pharmaceutical material, Steroid hormone, Anabolin. Is a male hormone, anabolic hormones drugs.
Durabolin Standard: USP28; BP2003
Storage: Shading, Confined Preservation
Package: Discreet Packing ways for your choice.
Delivery: Deliver out within 24 hours after payment.
Payment: West Union, T/T, Money Gram.
Deca Durabolin,also known as Nandrolon Decanoate, is perhaps the second-best known injectable anabolic androgenic steroid after Testosteron. Used for bulking.Nandrolon is the base hormone, but it is better known under the trade name Deca Durabolin, which contains Nandrolon Decanoate. This popular preparation takes the nandrolon hormone and adds a decanoate ester chain. This ester chain is attached during the manufacturing process and it serves dual purposes. The main purpose is to make the hormone oil soluble, so it can be put in an amp or multi-dose vial. The second purpose of this ester chain is to slow-release the steroid by keeping deca from interacting with androgen receptors until the ester chain is cleaved off by enzymes in your body. Since nandrolon decanoate cannot attach to an androgen receptor until enzymes in your body have cleaved off the decanoate ester, it causes the steroid to slow-release into your system over many days. For medical use, the ester's main function is to allow the hormone to be injected only once every 3 weeks. However, bodybuilders may inject deca durabolin weekly or as often as every three days.
Nandrolon decanoate can be used for the treatment of osteoporosis, for the palliative treatment of selected cases of disseminated mammary carcinoma in women and as an adjunct to specific therapies and dietary measures in pathologic conditions characterized by a negative nitrogen balance.
Nandrolon decanoate is an injectable sort of the anabolic steroid nandrolon. The decanoate ester supplies a slow release of nandrolon from the site of injection, continuation for up to 3 weeks. Nandrolon 200 USP injection provides nandrolon decanoate. In human trials nandrolone has been shown to positively influence calcium metabolism and to increase bone mass in osteoporosis. The esterification of the 17-beta-hydroxyl group increases the duration of the action of nandrolon. Nandrolon esters in oil injected intramuscularly are absorbed slowly from the lipid phase, thus Nandrolon 200 can be administered at intervals of 3-4 weeks. Nandrolon 200 contains nandrolone decanoate in a 10ml solution for injection (200mg nandrolon decanoate / ml). Nandrolon 200 is a yellowish oily solution for intramuscular injection.
Deca for 5 grams 25 ml @ 200mg/ml
5 grams powder
16.25ml sesame oil
1.25ml BA 5%
3.75ml BB 15%
Hot Sale Semi-finished Steroid Liquid
250mg/ml / 300mg/ml
250mg/ml / 300mg/ml
Testosteron Sustanon 250
200mg/ml / 250mg/ml
Testosteron Supertest 450
Nandrolon Decanoate (DECA)
200 / 250 / 300mg/ml
Drostanolone Propionate (Masteron)
Boldenon Undecylenate (Equipoise)
200mg/ml / 300mg/ml
Methenolon Acetate (Primobolone)
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