spec sheet11 rows
CL-316243 is a highly selective beta3-adrenergic receptor agonist and one of the most widely used research tools for studying fat loss, thermogenesis, and the browning of white fat. In animal models it powerfully triggers lipolysis, boosts energy expenditure, and improves glucose control. For metabolic and adipose tissue research, CL-316243 is a gold-standard beta3 agonist.
- Gold-standard beta-3 agonist in fat research
- Fires up brown fat and heat production
- Lipolysis triggered, fatty acids released for burning
- Turns white fat toward a fat-burning phenotype
- Whole-body energy expenditure climbs in rodent models
- Exceptionally selective for the beta-3 receptor
- Beta3 activation can transiently affect insulin and glucose levels
- Cardiovascular effects are possible with adrenergic agonists
Overview
CL-316243 is a synthetic, highly selective agonist of the beta3-adrenergic receptor (beta3-AR), a receptor subtype expressed prominently on white and brown adipocytes that controls lipolysis and thermogenesis [1][2]. Chemically it is a benzodioxole dicarboxylate compound, and it is one of the most selective beta3-AR agonists available, which is why it has become a standard experimental probe for dissecting beta3 signaling in fat tissue [1].
The compound was developed during pharmaceutical efforts to exploit the beta3-adrenergic receptor as an anti-obesity and anti-diabetic target, since activating this receptor increases metabolic rate through fat breakdown and heat production while also influencing insulin secretion and food intake [1]. Although it has been studied extensively in rodents, CL-316243 is used primarily as a research compound rather than an approved human medicine, and species differences in beta3-AR pharmacology have historically complicated translation to human therapeutics [1].
In research it is applied to study lipolysis, non-shivering thermogenesis, the browning or beiging of white adipose tissue, mitochondrial biogenesis, and glucose and lipid metabolism [3][4][6]. It is also a common tool for probing how these responses change with age or genetic manipulation [5]. Regulatory status is that of a research chemical; CL-316243 is not an approved therapeutic and is supplied for laboratory use, typically as a water-soluble powder or solution.
- CL-316243 is more than ten-thousand-fold selective for the beta3 receptor over the beta1 and beta2 subtypes in rodents, making it one of the cleanest adrenergic tool compounds available.
- In mice lacking white adipose tissue, the drug's dramatic metabolic effects vanish, showing that its actions are launched directly at the fat cell.
- The very species difference that doomed CL-316243 as a human drug, its weak activity at the human beta3 receptor, is what kept it thriving as a rodent research staple.
Mechanism
CL-316243's central benefits, as demonstrated in animal research, are potent fat mobilization, increased energy expenditure, and improved metabolic parameters, all driven through selective activation of the beta3- receptor. On engaging beta3-AR, the receptor raises intracellular cyclic AMP and activates protein kinase A, which phosphorylates hormone-sensitive lipase to break down stored triglycerides and release free fatty acids and glycerol [3][6]. In parallel it induces uncoupling protein 1 (UCP1) in brown and beige adipocytes, the molecular engine of non-shivering thermogenesis that burns fatty acids to produce heat [2][5].
The quantitative effects are striking. In wild-type mice, a single dose of CL-316243 produced roughly a 2-fold increase in serum free fatty acids, a 53-fold increase in , and a 2.4-fold decrease in glucose, effects that were completely absent in mice lacking white adipose tissue, demonstrating that the drug's actions are initiated at the adipocyte [1]. Chronic beta3 stimulation reduces fat mass and body weight, suppresses leptin, and induces UCP1 and biogenesis in fat depots [5]. Genetic studies confirm the pathway: the anti-obesity effect of beta3 stimulation is largely attributable to UCP1, and downstream signaling proceeds through both PKA-dependent and PKA-independent routes such as the Epac1 to p38gamma to NFAT5 axis [2][6].
A hallmark of CL-316243 in modern research is its ability to drive the browning of white adipose tissue, converting energy-storing white fat toward a thermogenic, brown-like phenotype rich in mitochondria [3][4]. This browning, together with enhanced fatty acid oxidation and improved glucose tolerance, is why the compound is a favored model for studying metabolic health, obesity, and diabetes [4][6]. The effects are highly receptor-specific, which gives CL-316243 its value as a clean pharmacological tool for the beta3 pathway [1].
receptor fingerprint
Beta-3 receptorSelective agonist activation on fat cells
UCP1 and brown fat thermogenesisInduces uncoupled respiration for heat
White adipose browningPromotes brown-like phenotype in white fat
Safetyrisks and cautions, not medical advice
CL-316243 is a selective beta-3 adrenergic receptor agonist used mainly as a laboratory research tool for fat loss and metabolism; it has essentially no human safety data and is sold as a research chemical. Its effects are inferred from its class rather than clinical study: beta-3 agonism could plausibly affect heart rate and blood pressure, and its off-target activity and long-term effects in humans are unknown.
History
CL-316243 was developed in the early 1990s by American Cyanamid's Lederle Laboratories as a highly selective agonist of the beta3-adrenergic receptor, and it was characterized in influential pharmacology reports by Bloom and colleagues around 1992. The original ambition was therapeutic; because beta3 receptors are enriched in fat tissue, the compound was pursued as a potential anti-obesity and anti-diabetic drug that could burn fat and improve glucose handling without the cardiovascular effects of beta1 and beta2 stimulation.
Human development ultimately disappointed, largely because rodent and human beta3 receptors differ, and CL-316243 is far more potent at the rodent receptor. Rather than fading away, the molecule found an enduring second life as a research tool, and it is now one of the most widely used pharmacological probes for the beta3 pathway. It has been central to the modern understanding of brown fat, beige adipocytes, and the browning of white adipose tissue.
Reputation
Within metabolic and adipose-tissue research, CL-316243 is treated as a gold-standard beta3 agonist and a remarkably clean pharmacological instrument. Investigators value its extreme receptor selectivity, which lets them isolate beta3 biology from the confounding effects of other adrenergic receptors, making it a reference compound for studies of lipolysis, thermogenesis, and mitochondrial biogenesis. It played a defining role in establishing the concept of beige or brite fat and in demonstrating that energy-storing white fat can be pushed toward a thermogenic, brown-like state. The honest caveat is that its story is one of laboratory success rather than clinical translation; because the human beta3 receptor responds poorly to it, CL-316243 is a tool compound and not a human therapeutic. That limitation is precisely why it remains prized as a specific, dependable probe.
Subjective profileweighing the evidence above
A lab reagent, not a fat-loss product. The dramatic browning and thermogenesis results are rodent results, human beta-3 pharmacology differs from the rat's, and there is essentially no human safety data. Nothing here to buy.
Where to buy
Suppliers
Vendors carrying CL-316243, with live product details and codes. Links are affiliate links that support the wiki at no cost to you.
Kimera Chems
CL-316243
Research
- 1999first citedBeta3-adrenergic regulation of leptin, food intake, and adiposity is impaired with age
- 2025most recentEpac1 mediates thermogenesis and lipolysis in white adipose tissue via the p38γ-NFAT5 axis in a…
- 1.Lack of responses to a beta3-adrenergic agonist in lipoatrophic A-ZIP/F-1 mice
- 2.Indispensable role of mitochondrial UCP1 for antiobesity effect of beta3-adrenergic stimulation
- 3.AHNAK deficiency promotes browning and lipolysis in mice via increased responsiveness to β-adrenergic signalling.
- 4.Oleoylethanolamide enhances β-adrenergic-mediated thermogenesis and white-to-brown adipocyte phenotype in epididymal white adipose tissue in rat.
- 5.Beta3-adrenergic regulation of leptin, food intake, and adiposity is impaired with age
- 6.Epac1 mediates thermogenesis and lipolysis in white adipose tissue via the p38γ-NFAT5 axis in a PKA-independent manner.
6 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
What does beta-3 selective mean?
It activates mainly the beta-3 adrenergic receptor on fat cells while largely sparing beta-1 and beta-2, which is why it is used to study fat burning specifically.
Does it burn fat?
In rodents, yes; it strongly turns on brown fat and lipolysis, and its anti-obesity effect depends heavily on the uncoupling protein UCP1.
Does it work the same in humans?
Not necessarily; rodent beta-3 receptors respond strongly and human fat biology differs, so the effect does not translate cleanly.
Limitations of the evidence
- Human beta3-receptor pharmacology differs from rodents
Adverse effects
- Beta3 activation can transiently affect insulin and glucose levels
- Cardiovascular effects are possible with adrenergic agonists
Notes and cautions
- Primarily a research compound; not an approved human medicine