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Cardarine (GW501516) – Results, Clinical Trials & Reviews

Cardarine (GW501516) is a PPARδ receptor agonist that was developed for the potential treatment of metabolic diseases and cardiovascular diseases [R, R].

Cardarine is purported by many recreational users to be the most effective endurance boosting chemical on the planet right now.

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What Is Cardarine?

Cardarine, also known as GW501516, is a peroxisome proliferator-activated receptor delta (PPARδ) agonist.

Cardarine is commonly lumped into the same category as selective androgen receptor modulators (SARMs) like Ostarine, but it is not a SARM at all.

SARMs, like Ostarine, are androgen receptor ligands that stimulate androgen receptors in a selective way, whereby they induce a significantly greater amount of anabolic activity in the body relative to androgenic activity [R].

Cardarine was designed by Ligand Pharmaceuticals and GlaxoSmithKline in the 90's.

It was initially intended as a potential treatment for metabolic diseases and cardiovascular diseases, but was ultimately abandoned in 2007 when animal testing revealed that it was either directly or indirectly related to the rapid development of cancerous tumors in multiple organs in both mice and rats [R].

Despite Cardarine's abandonment due to safety concerns, impressive performance enhancing benefits were noted in data that emerged from the tests.

The results were widely discussed in popular media, which caught the attention of many athletes.

Individuals seeking a competitive edge started to use Cardarine to improve their endurance. 

Recognizing this, the World Anti-Doping Agency (WADA) developed a detection test for GW501516 and other related PPARδ modulators, and shortly thereafter in 2009 it was added to their prohibited substance list [R, R].

Cardarine Potential Clinical Applications

Prior to 2007 (when Cardarine was abandoned), Cardarine was being investigated for its potential applications in treating metabolic diseases and cardiovascular diseases.

After undergoing preclinical trials and examining Cardarine's efficacy, the scope of its potential therapeutic applications narrowed as targets were set for phase 1 clinical trials.

The first target set was the treatment of hyperlipidemia, as Cardarine exhibited a profoundly positive reduction of triglycerides, fatty acids, VLDL, LDL, with a simultaneous increase in HDL (“good cholesterol”).

Other studies focused on the treatment of obesity, diabetes, dyslipidemia and cardiovascular disease occurred after 2003 on the back of positive results found in Phase 1 and Phase 2 trials in 2000-2002.

Had it not been for the studies revealing cancer development in mice and rats that were administered high doses of Cardarine, this chemical very likely would have progressed into further human trials, and perhaps even been approved for the treatment of a handful of metabolic disorders today.

Mechanism Of Action

Cardarine is a selective agonist of the PPARδ receptor.

It has a high affinity and potency for peroxisome proliferator-activated receptor delta [R].

Cardarine's Binding Affinity and Potency for PPAR Delta

Cardarine binds to PPARδ and recruits the coactivator PGC-1α.

Via activating PPARδ, the liver switches its energy source from glucose to fatty acids, which can in turn reduce blood sugar levels [R].

This in turn upregulates the body's expression of proteins involved in energy expenditure, improves insulin sensitivity and body composition, which can lower the overall incidence of type II diabetes and cardiovascular disease [R, R].

Cardarine Mechanism Of Action

Naturally, the first thing people started to associate Cardarine with is “exercise in a pill”.

Exercise mimetics would obviously be an extremely attractive alternative for many individuals, and delving further into the GW501516 data supports that the activation of PPARδ can in fact replicate many of the benefits gained from exercise itself.

Increased energy, muscle building potential, insulin sensitivity, fat burning potential, endurance, and improved lipid profiles are the most notable benefits that Cardarine has exhibited in testing via its selective activation of PPARδ [R].

Despite the array of blatant health benefits, Cardarine was ultimately dubbed a “failed exercise mimetic” as it was shown to promote cancer cell growth in animal studies [R, R].

Cardarine Clinical Trials

Preclinical Rat And Mice Models

In rats and mice treated with Cardarine, increased fatty acid metabolism in skeletal muscle and protection against diet-induced obesity and type II diabetes was observed.

In a metabolomic study of Cardarine for enhancing running endurance in Kunming mice, significant improvements were noted in the treated mice.

Cardarine treatment enhanced running endurance and the proportion of SDH-positive muscle fibres in both trained and untrained mice [R].

The effects of GW501516 on SDH-positive fibres in skeletal muscle of sedentary and trained KM mice
The effects of GW501516 on SDH-positive fibres in skeletal muscle of sedentary and trained KM mice

The increased running performance in Kunming (KM) mice occurred regardless of training, and the magnitude of improvement between both trained and sedentary treated mice was surprisingly high [R].

Running distance nearly doubled in the mice treated with Cardarine.

The effects of GW501516 on running performance in sedentary and trained KM mice. Forced wheel running endurance tests were performed following 3 weeks of treatment. (a) shows the total distance ran by mice in each group.
The effects of GW501516 on running performance in sedentary and trained KM mice. Forced wheel running endurance tests were performed following 3 weeks of treatment. (a) shows the total distance ran by mice in each group.

Other data further supports that PPARδ activation can regulate muscle fiber specification, and produce profound increases in long-distance endurance [R].

Other preclinical rodent models noted less commonly referred to benefits that should still be noted as they could have significant potential therapeutic applications in a clinical setting.

  • Cardarine lowered inflammation in mice [R, R, R]
  • Cardrine improved blood flow in mice by increasing nitric oxide levels, which can help prevent blood clots and other detrimental cardiovascular complications, as well as improve wound healing [R, RR]
  • PPARδ activation via Cardarine may help reverse obesity and diabetes by increasing total oxidative metabolism in white adipose tissue [R, R]
  • Cardarine significantly improved insulin sensitivity in mice, which is one of the main precursors to diabetes, obesity, heart disease and cancer. Improving blood glucose metabolism and preventing insulin resistance is one of the most important factors when it comes to maximizing vitality and longevity [R, R].

Preclinical Primate Model

A preclinical trial was conducted on obese rhesus monkeys, as they have a lipid profile that closely matches humans.

Cardarine increased HDL cholesterol, lowered LDL cholesterol, and reduced serum insulin levels [R].

No adverse effects were noted, and all health outcomes of this trial were positive.

The data in this preclinical model suggests that Cardarine could potentially be a very strong candidate in a clinical setting for lowering the occurrence of heart disease associated with metabolic syndrome [R].

The number 1 killer of humans that can be controlled via diet, exercise and chemical enhancement is heart disease, and any advancements in the niche of cardiovascular disease prevention would likely be a huge benefit for every one.

While Cardarine certainly wouldn't have been a complete fix for insulin resistance, inflammation, and arterial plaque build up, the data suggests that it potentially could've given patients a fairly significant edge in recalibrating their bodies to an insulin sensitive state with a more balanced lipid profile [R].

Phase 1 Trials

Two early Phase 1 trials in healthy subjects demonstrated the efficacy of Cardarine in reducing Triglycerides, LDL cholesterol, apoB and insulin levels and improving HDL cholesterol and insulin sensitivity [R, R].

First Phase 1 Human Trial

The first clinical trial was conducted on 24 healthy men for 2 weeks.

Each volunteer was either given placebo, 2.5 mg Cardarine, or 10 mg Cardarine per day.

Cardarine significantly improved HDL Cholesterol levels and reduced Triglycerides [R].

These lipid profile improvements are a result of Cardarine's ability to induce the upregulation of human skeletal muscle fat utilization, ABCA1 expression and enhanced serum fat clearance rates.

A fat feeding study was conducted where subjects were fed a high-fat breakfast on days 0 and 13 of the study 1 hour after taking their daily Cardarine dosage.

Triglyceride analysis was performed to assess how much (if at all) Cardarine would influence how efficiently the body processed those fats and how much nutrient partitioning in general was enhanced.

Lipolytic activity was gauged to assess the efficacy of Cardarine relative to placebo and the data revealed that the placebo group's Triglyceride levels went up significantly from high-fat meals, and the 2.5 mg and 10 mg treated groups both respectively lowered Triglyceride levels, even in the presence of the fat dense meals.

Cardarine Fat-Feeding Study Phase 1

Cardarine was shown to be safe and well-tolerated during this trial [R].

Subjects treated with Cardarine did not experience any significant adverse effects, including muscle and liver responses.

Liver enzymes and muscle proteins were measured to assess any potentially negative effects deriving from Cardarine.

None were found.

Second Phase 1 Human Trial

Most notably, the second Phase 1 trial found that Cardarine significantly reduced hepatic fat content by 20% [R].

The preclinical rodent models where over-expression of PPARδ was stimulated with Cardarine suggest improvements in metabolic syndrome reversal via enhanced fat oxidation in skeletal muscle.

This second phase 1 clinical trial sought out to replicate this result in humans.

10 mg per day was given to six healthy, moderately overweight subjects for 2 weeks.

Treatment with Cardarine showed statistically significant reductions in fasting plasma triglycerides, apolipoprotein B, LDL cholesterol, and insulin [R].

HDL cholesterol remained unchanged.

Fasting and postprandial plasma triglyceride and NEFA concentrations before (○) and after (•) drug treatment. A mixed meal was given at time 0.

A 20% reduction in liver fat content and a 30% reduction in urinary isoprostanes were also noted [R].

 Baseline characteristics of anthropometry, plasma biochemistry, liver enzymes, liver fat content, and urinary isoprostanes in the groups after randomization

Change from baseline to 14 days in fasting plasma biochemistry, liver enzymes, and urinary isoprostanes

The relative proportion of exhaled Carbon dioxide from the fat content of the meal was increased as a result of Cardarine administration, and skeletal muscle expression of CPT1b was also significantly increased [R].

Ratio (after/before) of CPT1B, ACAB, and PPARD mRNA content in skeletal muscle in response to placebo, GW590735, and GW501516 treatment

Cardarine successfully reversed multiple abnormalities associated with metabolic syndrome without increasing oxidative stress (one of the only negative side effects found in mega-dosed preclinical animal studies) [R].

The results of this second phase 1 trial looked very promising for potential therapeutic applications in a clinical setting to treat metabolic syndrome.

Phase 2 Trials

First Phase 2 Human Trial

The first phase 2 trial intended to examine the effect of Cardarine on lipoprotein metabolism.

The trial was conducted on 13 dyslipidemic men with central obesity who were administered with placebo or 2.5 mg of Cardarine per day.

The results confirmed Cardarine's lipid-modifying effects in dyslipidemic subjects with abdominal obesity, and also provided evidence of its effects in modulating lipoprotein kinetics (increase in catabolism of VLDL and pro- duction of apoA-I and apoA-II; decrease in production of apoC-III and LDL-apoB) [R].

GW501516 was also associated with a decrease in cholesteryl ester transfer protein activity but had no effect on insulin resistance [R].

Mean VLDL, IDL, LDL, and HDL triglyceride (A) and cholesterol (B) content ± SEM during placebo (closed square) and GW501516 (open square).
Mean VLDL, IDL, LDL, and HDL triglyceride (A) and cholesterol (B) content ± SEM during placebo (closed square) and GW501516 (open square).

The first phase 2 trial results further supported Cardarine's potential as a treatment of dyslipidemia in obesity [R].

Second Phase 2 Human Trial

In the second phase 2 trial, Cardarine or placebo was administered to 268 patients with low HDL cholesterol levels for 12 weeks [R].

Dosages of 2.5 mg, 5 mg, or 10 mg were administered to the treated patients.

A second smaller exploratory study in a similar population was conducted on 37 patients using a sequence of 5 and 10 mg dosing for the assessment of lipoprotein particle concentration [R].

Olson et al. reported that Cardarine treatment in this trial was associated with significant improvements in multiple lipid profile components (TG, LDL-C, HDL-C, free fatty acids and apoB, apoA-I and apoA-II) and a shift in LDL particle size from small dense to larger, less dense particles [R].

Low-density lipoprotein cholesterol (LDL-C) response over time by treatment group.
Low-density lipoprotein cholesterol (LDL-C) response over time by treatment group.
High-density lipoprotein cholesterol (HDL-C) response over time by treatment group.
High-density lipoprotein cholesterol (HDL-C) response over time by treatment group.
Free fatty acid (FFA) response over time by treatment group.
Free fatty acid (FFA) response over time by treatment group.

Despite the promising results found in Cardarine's preclinical, phase 1 and phase 2 trials, the further investigation and development of it was discontinued after observations in a couple rodent models found rapid cancer cell growth in the liver, stomach, tongue, skin, bladder, ovaries, womb and testes [R, R].

A summary of new PPAR agonists and SPPARMs in development

Cardarine Results (Anecdotal/Recreational Reports)

Endurance

Cardarine stimulates fatty acid metabolism and suppresses glucose catabolism without negatively affecting mitochondrial content or muscle fiber type.

By sparing glucose in the body, Cardarine delays the onset of hypoglycemia during exercise and substantially improves running times and overall endurance.

The massive boost in endurance is without a doubt the number one reported benefit of Cardarine, and it isn’t uncommon for users to rave about how their endurance feels like it has gone up 25-30% shortly after taking it.

Expectedly, athletes in endurance sports using Cardarine report very favorable outcomes in their performance.

Cardarine is unique in that it is one of the few chemicals suited more to enhancing athletic performance in a sports setting, rather than in a bodybuilding capacity. 

Athletes commonly report a very substantial increase in their ability to push past endurance plateaus where they would normally gas out.

Greater output in the gym, less required rest time, better running times, better hiking times, even better endurance in bed are all things commonly reported by recreational Cardarine users.

Fat Burning

Greatly accelerated fat loss is a commonly reported benefit of Cardarine, however, I believe it is far less potent than what some articles imply.

Anecdotally, I have yet to see any evidence of substantially increased fat loss derived solely from Cardarine.

By stimulating fatty acid oxidation via increasing glucose uptake, your body will resort majorly to stored fat as its energy source, and in turn improve fat burning potential.

This is what Cardarine aims to accomplish, and I believe to some extent it does, however, it is not a game changer in a bodybuilding context.

Muscle Growth

While Cardarine evidently exhibits some anti-catabolic properties, it does not yield significant hypertrophy in a bodybuilding context.

While it likely could be an effective tool for staving off fat gain, I do not believe that Cardarine has any substantial muscle building properties in humans.

My Cardarine Review

I feel that the fat burning capabilities of Cardarine are exaggerated and are typically only found in articles written by individuals who want to convince you to buy it.

Personally, I feel that Cardarine proves most useful as a cardiovascular endurance aid, or a modulator of lipids.

For all other purposes (fat loss, muscle growth, etc.) I feel like it falls short of it being worth using when we don't have definitive human data to conclude that it is definitely not going to accelerate cancer cell growth.

Do I think it causes cancer at commonly used dosages?

Based on what I've learned I think it is unlikely, however, I don't compete in endurance sports, nor do I feel the need to artificially boost my current endurance.

I do see very promising potential benefits in regards to its effects on insulin sensitivity and lipids, as chronically low HDL levels are extremely common among bodybuilders, even those on low TRT dosages.

With that being said, I still see it as a last resort even when it comes to lipids management.

My educated guess is that even synthetic GH usage (commonly used in bodybuilding without considering the implications) would probably be a far more risky cancer causing agent than Cardarine, but obviously the less things that can potentially cause cancer cell proliferation in your body the better.

I do not use Cardarine myself, and probably will not use it unless my HDL levels prove to be a significant detriment to my health long term, in which case I may consider it for lipids modulation.

Cardarine Dosage

Doses of 2.5 – 10 mg per day were used for up to 12 weeks in clinical trials.

Anecdotally, users report improved outcomes at a daily dosage of 10 – 20 mg per day with no serious adverse effects.

Half-Life

Cardarine's half-life was never revealed in the clinical data, however, in all human trials a once per day dosing frequency was used.

Based on that, we can assume that the half-life of Cardarine is ~ 24 hours.

Cardarine remains detectable in urine up to 40 days after a single oral dose of 15 mg [R].

Side Effects

Does Cardarine Cause Cancer?

At the 48th Annual Meeting of the Society of Toxicology in 2009 (2 years after Cardarine's abandonment), data was presented showing that Cardarine caused cancer to develop rapidly in several organs in animal testing [R].

The first thing to note is the fact that the aforementioned study involved administering Cardarine to Han Wistar rats for almost 2 years straight (1.99 years to be exact).

Without being administered any chemicals at all, the median life expectancy of Han Wistar rats is between 30 and 33 months for females, and between 33 and 36 months for males.

The reason for their short life expectancy is the number of adenocarcinomas that they develop [R].

Prior to even looking at the animal models for Cardarine, we know that these rats are not expected to live longer than 3 years already, irrespective of what they are administered, due to their high probability of developing cancer.

The dosages administered to rats over the 2 year study varied widely.

The lowest dosage showing cancer cell proliferation in an animal model being 3 mg/kg/day in Han Wistar rats for a period of 104 weeks [R].

The average weight of a Han Wistar rat is 509 grams, or 0.509 kg [R].

Average body weight of male Wistar rats.
Average body weight of male Wistar rats

The following equation is used to calculate roughly what that dosage would equate to in humans:

HED (mg / kg = Animal NOAEL mg/kg) × (Weightanimal [kg]/Weighthuman [kg])(1–0.67) [R].

Assuming we have an 80 kg man that we are using for this calculation, we get the following result:

Human Equivalent Dose = (3) × (0.509/80)(1–0.67)

Human Equivalent Dose = (3) x (0.0063625)(0.33)

Human Equivalent Dose = 3 x 0.18845044723

Human Equivalent Dose = 0.5653513417 mg/kg

Human Equivalent Dose For An 80 Kilogram Man = 45.2281073363 mg

Recreationally, the standard dosage is between 10 – 20 mg per day, which is not incredibly far off from the minimum human equivalent dosage to yield accelerated cancer development in the aforementioned rodent model.

Anecdotally, Cardarine has been shown to be generally well tolerated.

A study examined the effect of ligand activation of PPARβ/δ on cell proliferation, cell cycle kinetics, and target gene expression in human HaCaT keratinocytes using Cardarine and found that ligand activation of PPARβ/δ inhibits keratinocyte proliferation through PPARβ/δ-dependent mechanisms [R].

Keratinocyte carcinoma (skin cancer) is by far the most common cancer in the United States [R].

The ligand activation study provides strong data to support that Cardarine has the ability to inhibit cancer cell growth, rather than accelerate it.

In addition, in all of the clinical studies conducted on humans using dosages as high as 10 mg per day for 12 weeks, no serious adverse effects or cancer development was reported [R, R, R].

As of now, there is zero evidence to support that Cardarine use at the dosages used in human trials will cause cancer, however, it is certainly still possible.

Potentially Increased Cell Death

Reducing oxidative stress may increase protection from cell death, therefore measuring reactive oxygen species (ROS) levels may be a way to track cell death progression, or lack thereof.

CCl4-treated hepatocytes incubated with KD3010 (another PPARδ agonist) had reduced levels of ROS, whereas hepatocytes incubated with GW501516 showed more ROS production.

Via increasing ROS production, Cardarine increased starvation-induced cell death in cultured hepatocytes and exacerbated liver damage [R].

How Does Cardarine Stack Up To Other Endurance Boosting Chemicals

Cardarine Vs SR9009

SR9009 (also known as Stenabolic) is a synthetic Rev-ErbA ligand, not a SARM, although it is very commonly lumped into the SARMs category.

SR9009 works by increasing the mitochondria count in the muscles, resulting in a blatant improvement in endurance.

It causes no testosterone suppression, and there are no serious adverse events reported to date from SR9009 usage.

SR9009 has very poor bioavailability, making it useless in comparison to orally administered Cardarine, however, when SR9009 was injected into mice the results were very promising [R].

Pharmacological activation of Rev-erb-α substantially increased the running capacity and mitochondrial respiration of the mice in the preclinical model [R].

Yielding any performance outcomes with SR9009 would need to be achieved via injection only, as oral administration has proved an extremely low level of bioavailability, and there are no current human trials.

Anecdotally, we can only assume that Cardarine has a greater overall efficacy profile than SR9009, however, this may not be the case, as the very few cases of intravenously administered SR9009 have reportedly yielded positive outcomes (do not try this obviously).

Cardarine Vs EPO

Recombinant human erythropoietin (EPO) is a glycoprotein hormone produced by the interstitial fibroblasts in the kidney that signal for erythropoiesis in bone marrow.

One of the main effects of EPO is increased red blood cell production and the elevation of hematocrit levels.

EPO became a heavily abused drug by amateur and professional cyclists because of its ability to significantly improve exercise performance [R].

Serious adverse events are reported far more often with EPO than with Cardarine.

While there has never been a clinical study comparing its efficacy and safety profile to Cardarine (and there likely never will), EPO is significantly more dangerous in both the short and long term.

Arterial hypertension, cerebral convulsion/hypertensive encephalopathy, thrombo-embolism, iron deficiency and influenza-like syndrome have all been commonly reported adverse events occurring with long term EPO usage [R].

To date, there are no adverse events that have been reported in human trials with Cardarine.

Keep in mind, the sample size of those human trials is small, and long term evaluations of those individuals have not been made to establish long term cancer risk.

In a performance enhancing context, you would be hard-pressed to find someone who believes EPO is a safer alternative to Cardarine.

Cardarine Vs Equipoise

Equipoise (Boldenone) is an anabolic androgenic steroid that is unique in that it stimulates the release of erythropoietin in the kidneys notably more so than other steroids [R].

Anything that increases red blood cell count and hematocrit will increase the potential for improved endurance during exercise, however, this comes with the risk of a myriad of dangerous cardiovascular outcomes.

Equipoise will also shut down natural testosterone production for the duration of its use, which is obviously not ideal for individuals who don't want to trade endocrine shutdown for an endurance boost.

Equipoise usage would need to be followed up with a PCT phase, whereas Cardarine and EPO wouldn't as they do not suppress endocrine function.

The mechanism of action by which Cardarine improves endurance is completely different than Equipoise, or EPO, and we can surmise has an overall greater safety profile both short term and long term.

With that being said, none of these chemicals are without risk.

Cardarine Bulking Cycle

In a calorie surplus Cardarine is reported to prevent fat accumulation, as well as maintain cardiovascular endurance by offsetting the body's increased oxygen requirements as it gains weight.

In a performance enhancing context, cycles like the following are commonplace among users.

MK-677 and SARMs like LGD-4033, RAD140 or S23 are commonly stacked alongside Cardarine in more involving performance enhancement bulking protocols.

Cardarine Cutting Cycle

In a calorie deficit Cardarine is reported to enhance fat burning potential and inhibit lean muscle breakdown.

For use in a performance enhancing context, cycles like the following are commonplace among users (the length of this may vary depending on the user's individual timeline constraints for reaching a goal body fat percentage).

SARMs like Ostarine, or S4 are commonly stacked alongside Cardarine in more involving performance enhancement cutting protocols.

PCT (Post Cycle Therapy)

Cardarine does not cause endocrine suppression, it doesn't lower natural testosterone levels, and it doesn't inhibit LH, FSH or SHBG.

It does not raise estrogen either, which has an indirect effect on testosterone suppression.

As Cardarine doesn't suppress any sex hormones, or increase any antagonizing hormones, there is no hormonal suppression that occurs via Cardarine use, and therefore would not require a PCT phase.

If a suppressive anabolic steroid or SARM was used concurrently with Cardarine, then that would require PCT.

Cardarine Used With Trenbolone To Offset Loss Of Cardiovascular Endurance

Trenbolone is notorious for severely crushing cardiovascular endurance and making it incredibly hard to complete sufficient cardio activity without getting winded extremely easily.

Cardarine has become very popular as of recent with Tren users as it is reported to mitigate the Tren cardio side effect, allowing the user to keep their endurance in top form while concurrently running Tren.

Buy Cardarine

Most Cardarine sources do not third party test their products, nor do they have any satisfactory level of quality control whatsoever.

I highly advise that before you buy SARMs or Cardarine from a company online you thoroughly evaluate their track record, their third party test results, and how they are marketing their products in general.

These Are My Current Trusted/Go To Companies For Third Party Tested 99%+ Pure Cardarine:

Disclaimer: The information included in this article is intended for entertainment and informational purposes only. It is not intended nor implied to be a substitute for professional medical advice. Prior to buying anything, check that it is compliant where you live with your current government laws.

39 thoughts on “Cardarine (GW501516) – Results, Clinical Trials & Reviews”

        1. Depends on the amount in the bottle and the dosage of each pill/ml. The correct question to ask is, “What dose/timing is most effective?”. Then do the math yourself.

  1. How much does the ability you gained on the cycle diminish when you go off? Ex, if you got down to a 5 minute mile on cycle, would you lose significant time coming off?

  2. How fast is GW out of your system? Im a NCAA athlete and get drug tested every month or so and dont want to get caught “doping”, but would still like to get a edge on the competition haha.

    1. Nobody knows, at best I could throw a general educated guess at you but it would probably be +/- several days based on the individual.

      If you are tested every single month like clockwork I probably wouldn’t risk it at all. Even though the half life is short, the detection time could be several weeks.

  3. I just began taking this and found I trained extra hard. Just curious to know , Does this trim down body fat and build muscle ? Can I get really toned and ripped on it.

    1. It doesn’t build muscle really, and the fat burning capabilities are typically exaggerated, it’s main benefit is the huge boost in endurance and positive effect it has on lipids. You can get toned and ripped on anything if your diet and cardio are in check.

  4. It does actually build muscle if you keep with it and it don’t take too long either. I do however agree with Derek that the fat burning capabilities are typically exaggerated.

  5. How long will last for 20mg? perday? i have coming race 400KM endurance challenge race, cut off time 80Hrs….. it is work for 80 hrs? mean i take continue for 4 days? 8 tablet? would it hurt kidney?
    the race in sahara…. .. any for you experience this?
    your sharing much appreciated..

  6. hey just a quick question derek!

    people say take 30 mins-1 hour before your work out, is there a specific reason why? Would the effects be different if I dose it all in the morning instead? Or does it somehow give you a “pump” if you take it 30mins -1 hour pre workout?

  7. Test run

    Start 180 days of mk677 15mg
    90 days in start mk2866 25mg for 90 days
    30 days of arimrx 75mg at end of mk2866
    90 days of cardarine 10mg to start two weeks before mk2866 ends

    Thoughts?

    1. I’d rotate to another anabolic at the 7 week mark if you’re going to run a short acting anabolic for 13 weeks straight.

          1. Short half-life. Orals with short half lives will typically result in stalling out progress at about the 7-8 week mark, hence the rotation method.

  8. I dont want to take Cardarine long-term.. if I use to break-through running plateau, will i be able to maintain that level?

  9. How long does it take before you can feel the difference in endurance?
    How does liquid compare to tablet, conversion wise, like 1ml would be how many grams?

  10. Pingback: Cardarine Underground Secrets: The World's Most Potent Fat Burner?

  11. https://www.researchgate.net/deref/http%3A%2F%2Fwww.fda.gov%2Fdownloads%2FDrugs%2FGuidances%2FUCM078932.pdf

    Please read page 7. The way you are doing your calculation is not doesn’t take the fat surface area into account. This link has the fda guidelines that simplify it for different species (including rats). The reality is that the cancerous dose is a lot closer to doses people are taking, and in some cases, forum posts indicate people are exceeding it. I’m not saying that it causes cancer in these smaller time frame cancer, but I am just saying that we really don’t know. Another limitation is that 3mg/kg is the lowest dose tested on the rats, so we don’t know what the floor is for the cancerous dose. IF they had tested 2mg/kg for example, that may have also been cancerous; or maybe not; point is that we don’t know what the floor is. I hope you respond and I honestly hope I’m proven wrong, because I would love to take this substance but I am scared of it. I’m studying pharm in Med school rn (1st year), so I’m not claiming to know everything, but I’m not research naive either. Regardless, I’m
    A big fan, and appreciate the knowledge you put out, but I hope you take this into account as well.

  12. Cardarine fucking works, the issue for me is that it can accentuate the side effects of Ostarine.

    When I was still in the Navy doing Andarine, Ostarine, Cardarine I could workout for like 2-3 hours straight and not get tired. Surpression was evident in using the three together and my hair would start to thin. To be honest Cardarine works very well by itself if used in the right dose for like a 4-6 week cycle.

    I had done the SARMS cycle on 25 mg of Ostarine, I’ll probably try it again at 12.5mg Ostarine plus Cardarine. Makes for a decent cutting cycle.

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