This is a working overview of GW501516, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2025-08-16. Anything still debated is marked as such rather than presented as settled.
The compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic PPARδ agonist | Not a steroid or a selective androgen receptor modulator. |
| Common synonyms | Cardarine, GW501516, GW-501516, endurobol | Names vary by supplier and literature source. |
| Appearance | White to off-white powder | Consistent with many small-molecule research chemicals. |
| Solubility | Low in water; soluble in DMSO and ethanol | Often prepared in organic solvent for laboratory work. |
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid and energy metabolism. |
Cardarine can be detected in biological samples and product materials using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The method separates compounds by chromatography and identifies them by mass-to-charge transitions, allowing low-level detection in urine or blood. Sample preparation often involves enzymatic hydrolysis, solid-phase extraction, or protein precipitation. Certified reference materials and isotope-labeled internal standards improve quantification. Detection windows depend on metabolism, matrix, and assay sensitivity, so no single universal window applies.
Regulatory treatment of cardarine differs by context and jurisdiction. In competitive sport, the World Anti-Doping Agency lists PPARδ agonists, including GW501516, as prohibited at all times. Outside sport, it lacks approval as a prescription medicine in major drug markets, and products sold for human consumption may be treated as unapproved drugs. Some countries also restrict importation or sale through general consumer protection and medicines laws. These classifications affect availability, testing, and legal risk without establishing therapeutic value.
Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.
Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.
In the early 2010s, the Manmohan Singh-led Indian government depended on the parliamentary support of the Communist Party of India (Marxist) which has led state governments in Kerala, Tripura and West Bengal. However, with the rise of Hindu nationalism, the communists continued to shrink in India and are currently only take power in the state of Kerala. The armed wing of the Communist Party of India (Maoist) has been fighting in the ongoing Naxalite–Maoist insurgency against the government of India since 1967 and is still active in East India. Sri Lanka has had Marxist–Leninist ministers in their national governments such as Janatha Vimukthi Peramuna and National People's Power with its Marxist leader Anura Kumara Dissanayake came to power in 2024. Maoist rebels in Nepal engaged in a civil war from 1996 to 2006 that managed to topple the monarchy there and create a republic. Communist Party of Nepal (Unified Marxist–Leninist) leader Man Mohan Adhikari briefly became prime minister and national leader from 1994 to 1995 and the Maoist guerrilla leader Prachanda was elected prime minister by the Constituent Assembly of Nepal in 2008. Prachanda has since been deposed as prime minister, leading the Maoists, who consider Prachanda's removal to be unjust, to abandon their legalistic approach and return to their street actions and militancy and to lead sporadic general strikes using their substantial influence on the Nepalese labour movement. These actions have oscillated between mild and intense.
=== Ovulation === NGF is abundant in seminal plasma. Recent studies have found that it induces ovulation in some mammals e.g. "induced" ovulators, such as llamas. Surprisingly, research showed that these induced animals will also ovulate when semen from on-schedule or "spontaneous" ovulators, such as cattle is used. Its significance in humans is unknown. It was previously dubbed ovulation-inducing factor (OIF) in semen before it was identified as beta-NGF in 2012.
== Contraindications == Dapoxetine should not be used in men with moderate to severe hepatic impairment and in those receiving CYP3A4 inhibitors such as ketoconazole, ritonavir, and telithromycin. Dapoxetine also cannot be used in patients with heart failure, permanent pacemaker, or other significant ischemic heart disease. Caution is advised in men receiving thioridazine, monoamine oxidase inhibitors, SSRIs, serotonin-norepinephrine reuptake inhibitors, or tricyclic antidepressants. If a patient stops taking one of these drugs, he should wait for 14 days before taking dapoxetine. If a patient stops taking dapoxetine, he should wait for 7 days before receiving these drugs.
For example, studies have identified TLR4 as the receptor for the LPS component of Gram-negative bacteria. TLRs are key regulators of both innate and adaptive immune responses. Unlike RelA, RelB, and c-Rel, the p50 and p52 NF-κB subunits do not contain transactivation domains in their C terminal halves. Nevertheless, the p50 and p52 NF-κB members play critical roles in modulating the specificity of NF-κB function. Although homodimers of p50 and p52 are, in general, repressors of κB site transcription, both p50 and p52 participate in target gene transactivation by forming heterodimers with RelA, RelB, or c-Rel. In addition, p50 and p52 homodimers also bind to the nuclear protein Bcl-3, and such complexes can function as transcriptional activators.
Sources: en.wikipedia.org
Combination of MAO-substrate psychedelics with monoamine oxidase inhibitors (MAOIs) can result in overdose and toxicity. Examples of MAOIs that may potentiate psychedelics behaving as MAO-A substrates, such as psilocin, include phenelzine, tranylcypromine, isocarboxazid, and moclobemide, as well as harmala alkaloids like harmine and harmaline and chronic tobacco smoking. An early clinical study of psilocybin in combination with short-term tranylcypromine pretreatment found that tranylcypromine marginally potentiated psilocybin's peripheral effects, including pressor effects and mydriasis, but overall did not significantly modify its psychoactive and hallucinogenic effects, although some of its emotional effects were said to be reduced and some of its perceptual effects were said to be amplified. Psilocin may be metabolized to a minor extent by the cytochrome P450 (CYP450) enzymes CYP2D6 and/or CYP3A4 and appears unlikely to be metabolized by other CYP450 enzymes. The role of CYP450 enzymes in psilocin's metabolism seems to be small, and so considerable drug interactions with CYP450 inhibitors and/or inducers may not be expected. Psilocin's major metabolic pathway is glucuronidation by UDP-glucuronosyltransferase enzymes including UGT1A10 and UGT1A9. Diclofenac and probenecid are inhibitors of these enzymes that theoretically might inhibit the metabolism of and thereby potentiate psilocybin's effects, but no clinical research or evidence on this possible interaction exists. Few other drugs are known to influence UGT1A10 or UGT1A9 function.
Agrobacterium tumefaciens overwinters in infested soils. Agrobacterium species live predominantly saprophytic lifestyles, so its common even for plant-parasitic species of this genus to survive in the soil for lengthy periods of time, even without host plant presence. When there is a host plant present, however, the bacteria enter the plant tissue via recent wounds or natural openings of roots or stems near the ground. These wounds may be caused by cultural practices, grafting, insects, etc. Once the bacteria have entered the plant, they occur intercellularly and stimulate surrounding tissue to proliferate due to cell transformation. Agrobacterium performs this control by inserting the plasmid T-DNA into the plant's genome. See above for more details about the process of plasmid DNA insertion into the host genome. Excess growth of the plant tissue leads to gall formation on the stem and roots. These tumors exert significant pressure on the surrounding plant tissue, which causes this tissue to become crushed and/or distorted. The crushed vessels lead to reduced water flow in the xylem. Young tumors are soft and therefore vulnerable to secondary invasion by insects and saprophytic microorganisms. This secondary invasion causes the breakdown of the peripheral cell layers as well as tumor discoloration due to decay. Breakdown of the soft tissue leads to release of the Agrobacterium tumefaciens into the soil allowing it to restart the disease process with a new host plant.
He also initiated the President's Emergency Plan for AIDS Relief, in 2003, to address the global AIDS epidemic. The September 11 attacks during 2001 decisively reshaped his administration, resulting in the start of the war on terror and the creation of the Department of Homeland Security. Bush ordered the invasion of Afghanistan in an effort to overthrow the Taliban, destroy al-Qaeda, and capture Osama bin Laden. He signed the Patriot Act, expanding surveillance powers for suspected terrorists. He also ordered the 2003 invasion of Iraq to overthrow Saddam Hussein's regime, citing claims that it possessed weapons of mass destruction and had ties with al-Qaeda. Bush later signed the Medicare Modernization Act, which created Medicare Part D. In 2004, Bush was re-elected president in a close race, beating Democratic opponent John Kerry and winning the popular vote. During his second term, Bush negotiated various free trade agreements, appointed John Roberts and Samuel Alito to the Supreme Court, and sought major changes to Social Security and immigration laws, both of which ultimately failed in Congress. He was widely criticized for his administration's handling of Hurricane Katrina and revelations of torture against detainees at Abu Ghraib prison in Iraq. Amid his unpopularity, the Democrats regained control of Congress in the 2006 elections. In January 2007, Bush launched a surge of troops in Iraq.
Sources: en.wikipedia.org
Cardarine is a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.
It binds to and activates PPARδ, a nuclear receptor that regulates genes related to fatty acid oxidation and energy use. This activation alters transcription in tissues such as skeletal muscle and liver. The full range of downstream effects in humans is not fully established.
No, cardarine is not known to occur naturally in plants, animals, or humans. It is a synthetic molecule produced for laboratory research. Products labeled as cardarine should therefore be treated as manufactured chemicals with variable purity.
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.