R.I.P E.D

109.99 $

Super concentrated formula

29


OSTARINE

20


S23

10


SR9011

20


GW501516

**These statements have not been evaluated by the Food and Drug administration (FDA). This product is not intended to diagnose, treat, cure, or prevent any disease.
*All amounts per 1Ml serving

R.I.P E.D formulation

Ostarine MK-2886 is an, non-steroidal Selective Androgen Receptor Modulator (SARM) with tissue-selective anabolic and androgenic pharmacologic activity. It is also known in the literature as enbosarm, GTx-024 or S-22.

Originally discovered in 1998, by James T. Dalton, Duane D. Miller, Karen A. Veverka, and their research teams at Ohio State University, the University of Tennessee, and GTx, respectively. GTx licensed the use of enbosarm from those research teams and further licensed the development of MK2886 with Merck and Co.

MK-2886 is one of the first SARMS to be synthesized and studied in rats and primates. As a result, it is one of the most extensively researched SARMS.

One study was performed on the cellular level of adult rats, specifically the adipocytes or fat cells. With the administration of MK-2886 Ostarine, the expression of fat-mediating hormones like leptin and adiponectin mRNAs was decreased. Because of these effects, researchers concluded that MK-2886 Ostarine was likely to behave similarly to testosterone on the AR receptors and decrease the body fat of the rat. Study.

In addition to fat loss potential, MK-2886 Ostarine has also been shown to stimulate bone growth in rats. One study removed a portion of the tibia from 4 groups of rats and then administered increasing levels of the SARM (0.04, 0.4, and 4mg/kg) over the course of 5 weeks. At the highest dosing level, 4mg/kg, the test subjects showed denser bone regrowth, increased healing time of the bone, and higher markers of bone growth hormones such as phosphorus and alkaline phosphatase.

Interestingly, all of the rats in the study group demonstrated an increased weight of the gastrocnemius muscle over rats who were not treated with MK-2886, even at the lowest dosing levels (0.04mg/kg, a decrease of 100 fold from the highest dosing group).

Serum cholesterol levels were also reduced in this treatment group and the median dose group (0.4mg/kg). The improved lipid profile of the mice was also noted in the earliest studies of MK-2886. Study.

Another study yielded similar results, with rats with clinically induced osteoporosis showing increased bone density in the long bones (such as the femurs, bone growth was not noted in the vertebrae) in rats treated at moderate to high levels of MK 2866. Study.

A third study specifically evaluated muscle growth in mice to evaluate the function of MK-2866 with mice who were genetically developed to be without traditional androgen receptors. Then by removing the mice’s endogenous testosterone-producing cells, they noted further muscle wasting and began MK-2886 treatment. These mice experienced muscle growth in androgen-sensitive muscles, indicating a separate pathway, distinct from sat ARKO that encouraged muscle growth at the same levels as DHT. – Study.

S23 is an orally available selective androgen receptor modulator or SARM. Originally developed by GTX as a form of hormonal male contraception in rats,it exhibits a high affinity for the androgen receptor with a Ki of 1.7 nM. Researchers, Jones et. Al published a research study comparing the effectiveness of S-23 in both castrated and intact male rats.

In castrated male rats, the effective dose of S23 in the prostate was 0.43 mg/d and 0.079 mg/d in the levator ani muscle. In intact male rats, doses greater than 0.1 mg/d of S-23 suppressed levels of luteinizing hormone (LH) by more than 50%. Furthermore, this dose of S-23 corresponded with decreased size of the prostate and increased size of the levator ani muscle Study. In intact males treated with S-23 as well as estradiol benzoate (to maintain sexual behavior), after 10 weeks there was no sperm found in the testis in four out of the six subjects and no reported pregnancies in all six of the subjects. After the treatment, infertility was completely reversed and 100% of the mating trials resulted in pregnancy.

The effects of S23 on muscle mass and body fat are comparable to the effects of anabolic steroids. In a study conducted in male rats it was discovered that while being treated with S23, the overall body weight and fat mass of the rats decreased. As it was previously mentioned, rats being treated with S23 were also given estradiol benzoate (EB) to maintain sexual behavior. EB is considered an estrogen which is known to cause muscle loss, however, when combined with S23 the effects of the estrogen were canceled out and the muscle mass of the male rats increased Study. . Additionally, in another study using rats, the effectiveness of S23 was tested against muscle loss due to long-term usage of glucocorticoids. This study also looked into the effects of S23 on castration-induced atrophy. In both cases, there was muscle loss but by supplementing S23 and testosterone to the rats the dexamethasone-induced dephosphorylation of Akt is blocked. Overall this study indicated that using S23 may be a more effective way of treating glucocorticoid-induced muscle loss Study.

SR-9011 is a research drug that was developed by Professor Thomas Burris of Scripps as an agonist of Rev-ErbAα with a half-maximum inhibitory concentration (IC50) = 790 nM for Rev-Erbα and IC50 = 560 nM for Rev-ErbAβ.[1] It has been used in the study of the regulation of the circadian rhythm and its links to immune system function, inflammation and cancer. SR-9011 is a second-generation activator of the Rev-ErbA receptors which are found abundantly in liver, skeletal muscle, fat tissue, and the brain.

GW-501516 is a PPAR agonist (peroxisome proliferator-activated receptor), originally developed for hyperlipidemia, obesity, metabolic dysfunction, and cardiac disease by GlaxoSmithKline, a multinational pharmaceutical company. The compound is known also by other names Endoburol, Cardarine, and is often used in research studies, cited as a PPARδ agonist. Various studies have shown GW-501516 to impact fatty acid metabolism, skeletal muscle endurance, and glucose/insulin balance. As PPARδ plays an important role in mitochondrial respiration, temperature regulation, inflammation mediation, skin and muscle repair, skeletal reprogramming, and keratinocyte differentiation, it can be assumed that GW501516 may have an impact on these additional areas. Study. . One mouse study clearly demonstrates the impact of GW5015016 in endurance levels of mice, both in trained and untrained mouse subjects. After three weeks of GW-501516, trained rats demonstrated a 31.2 percent increase in their total running distance, whereas untrained rats increased their total distance by 68.6 percent. Even one week of GW5015016 increased the running distance by 48.6 percent over the control group. Of the group that both received Cardarine and were previously trained to run, higher usage of longer saturated fatty acids, as well as triglycerides, were shown to enhance running endurance, likely due to increased fatty acid metabolism after PPARδ activation which up-regulates PDK4 and other mediating pathways of fatty acid oxidation. Study. . Molecular analyses revealed that PPARδ is involved in exercise-induced reprogramming of muscle fibers and skeletal muscle metabolism by regulating the expression of genes associated with contractile proteins, mitochondrial biogenesis, and lipid oxidation. Another study confirmed the above by administering GW501516 to mice who were fed a high-fat diet. The dosed group experienced only a slight weight loss but metabolic markers such as decreased insulin resistance, increased metabolic rate, increased mitochondria, and reduced lipids in skeletal muscle were noted. Additionally, glucose in plasma and insulin in blood was decreased in genetically obese mice. Study. . One study indicated that GW-501516 may also play a role in reducing inflammation, specifically in the liver. For rats fed a high fructose diet, GW-501516 reduced the inflammation markers ACE/AT1r axis. Additionally, it increased the genes that regulate beta-oxidation and decreased those that regulate fat cell and glucose creation. Study. . Similar results were noted in primate studies, a study of middle-aged, overweight to obese rhesus monkeys, indicated that HDL cholesterol was increased, LDL was decreased along with fasting triglycerides and fasted insulin levels. Researchers believed GW501516 could represent an important breakthrough for cardiovascular disease such as atherosclerosis and could reduce the severity of metabolic syndromes.Study. .

possible side effects

Not for human consumption, Please read the research papers related to this chemical before administration, Misuse of this product can result in dangerous side effects.