12
 min read

Asprosin Obesity Treatment: When Will It Be Available?

Written by
Bolt Pharmacy
Published on
24/2/2026

Asprosin is a hormone secreted by fat tissue that regulates blood sugar and appetite, with elevated levels observed in people with obesity. Whilst research into asprosin-targeted obesity treatments shows promise in animal studies, no such therapies are currently approved or in human clinical trials. This article examines asprosin's role in obesity, the current state of research into asprosin-blocking treatments, and the evidence-based obesity management options available through the NHS today. Understanding both emerging science and established treatments helps patients and clinicians make informed decisions about weight management.

Summary: Asprosin-targeted obesity treatments remain in early animal research with no human trials registered; no such therapies are expected to reach UK clinical practice for many years.

  • Asprosin is a hormone secreted by fat tissue that stimulates glucose production in the liver and may influence appetite regulation.
  • Elevated asprosin levels in obesity are associated with insulin resistance and impaired glucose metabolism.
  • Animal studies of anti-asprosin antibodies show reduced blood glucose, improved insulin sensitivity, and weight loss, but human safety and efficacy remain unknown.
  • No asprosin-targeted treatments are approved by the MHRA or in human clinical trials as of 2025.
  • Current evidence-based NHS obesity treatments include lifestyle interventions, medications (orlistat, semaglutide, liraglutide), and bariatric surgery for eligible patients.
  • Drug development from discovery to approval typically takes 10–15 years, requiring extensive safety testing and regulatory evaluation.
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What Is Asprosin and Its Role in Obesity

Asprosin is a relatively recently discovered hormone that has emerged as a significant area of interest in metabolic research. First identified in 2016, asprosin is a glucogenic protein hormone secreted primarily by white adipose tissue (fat cells) during fasting states. It functions as a signalling molecule that travels to the liver, where it stimulates the rapid release of glucose into the bloodstream, thereby helping to maintain blood sugar levels between meals.

In individuals with obesity, research has demonstrated that asprosin levels are often significantly elevated. This elevation appears to be associated with problematic metabolic changes: higher circulating asprosin concentrations are linked to excessive hepatic glucose production, contributing to insulin resistance and impaired glucose metabolism. Observational studies have shown that obese individuals may have substantially higher asprosin levels than those with healthy body weight, and these elevated levels have been associated with altered appetite and food intake in animal models.

The hormone's mechanism of action involves binding to receptors on liver cells—though the precise human receptor remains under investigation (animal studies have identified candidates such as OLFR734 in mice)—activating the cyclic AMP-protein kinase A pathway, which then triggers both gluconeogenesis (the production of new glucose) and glycogenolysis (the breakdown of stored glycogen). Beyond its effects on glucose metabolism, asprosin also appears to influence appetite regulation through actions on the hypothalamus in animal studies, the brain region responsible for hunger and satiety signals. This dual action—promoting both glucose production and appetite in experimental models—makes asprosin a particularly interesting target for obesity research.

Understanding asprosin's role has opened new avenues for investigating the complex hormonal dysregulation that characterises obesity. However, it is important to note that asprosin is just one component of the intricate network of hormones, including leptin, ghrelin, and insulin, that collectively regulate energy balance and body weight. The interplay between these various metabolic signals remains an active area of scientific investigation, and the extent to which findings from animal studies translate to human physiology requires further research.

Current Research on Asprosin-Targeted Treatments

Research into asprosin-targeted therapies remains in early experimental stages, with most studies conducted in laboratory settings and animal models rather than human clinical trials. Scientists have explored several potential therapeutic approaches, including the development of monoclonal antibodies that could neutralise circulating asprosin, thereby reducing its effects on glucose production and appetite.

In preclinical studies using mouse models of obesity and diabetes, anti-asprosin antibody treatments have shown promising results. These experiments demonstrated that blocking asprosin activity led to reduced blood glucose levels, improved insulin sensitivity, and decreased food intake, ultimately resulting in weight loss in the treated animals. However, it is crucial to emphasise that animal study results do not always translate directly to human physiology, and safety findings in animals cannot predict human safety profiles.

Another research direction involves investigating small molecule inhibitors that could potentially block asprosin's receptor or interfere with its signalling pathway in the liver. This approach might offer advantages in terms of oral bioavailability and manufacturing scalability compared to antibody-based therapies, though such work remains highly speculative at present.

The scientific community has also focused on understanding asprosin's structure and function at the molecular level. Detailed structural studies have revealed how asprosin interacts with its cellular targets in animal models, information that may prove essential for rational drug design. Additionally, researchers are investigating whether genetic variations in the gene encoding asprosin (the FBN1 gene) might influence obesity risk, though human genetic evidence remains limited and uncertain.

Despite these advances, as of 2025, there is no asprosin-targeted treatment approved for clinical use in the UK or elsewhere. The transition from laboratory research to human therapeutics typically requires extensive safety testing, dose-finding studies, and large-scale clinical trials—a process that generally takes many years and substantial investment. Searches of clinical trial registries (ClinicalTrials.gov, ISRCTN, EU Clinical Trials Register) have not identified any registered human trials of asprosin-blocking therapies to date.

Existing Obesity Treatments Available in the UK

While asprosin-targeted therapies remain experimental, several evidence-based obesity treatments are currently available through the NHS. The National Institute for Health and Care Excellence (NICE) provides comprehensive guidance on obesity management (NICE CG189), emphasising a tiered approach that begins with lifestyle interventions and progresses to pharmacological and surgical options for appropriate patients.

Lifestyle modification remains the foundation of obesity treatment. NICE recommends multicomponent interventions that address diet, physical activity, and behavioural change. These programmes typically involve regular contact with healthcare professionals over at least three months and aim for a realistic weight loss of 5–10% of initial body weight. Referral to specialist weight management services (tier 3 services) is generally appropriate for individuals with a BMI of 40 kg/m² or above, or 35 kg/m² or above with significant obesity-related comorbidities. Lower thresholds may apply for people from South Asian, Chinese, other Asian, Middle Eastern, Black African, or African-Caribbean backgrounds, who are at increased risk of obesity-related conditions at lower BMI levels.

Regarding pharmacological treatments, the MHRA has approved several medications for obesity management in the UK:

  • Orlistat (available both on prescription and over-the-counter as Xenical® or Alli®) works by inhibiting pancreatic lipase, reducing dietary fat absorption by approximately 30%. It is indicated for adults with a BMI of 30 kg/m² or above, or 28 kg/m² with associated risk factors. Prescribing information is available in the MHRA/EMC Summary of Product Characteristics.

  • Semaglutide (Wegovy®), a GLP-1 receptor agonist administered as a weekly subcutaneous injection, has recently become available for weight management. It works by reducing appetite and slowing gastric emptying. NICE recommends it (NICE TA875) for adults with at least one weight-related comorbidity and a BMI of 35 kg/m² or above (or 32.5 kg/m² for certain ethnic groups at higher risk), or in specific circumstances for those with a BMI of 30–34.9 kg/m². Treatment must be provided within a specialist weight management service and is limited to a maximum of two years.

  • Liraglutide (Saxenda®), another GLP-1 receptor agonist given as a daily injection, is licensed for weight management under more restricted criteria. NICE recommends it (NICE TA664) only for specific high-risk groups with nondiabetic hyperglycaemia and high cardiovascular disease risk, within specialist weight management services, and for a maximum of two years.

Bariatric surgery represents the most effective intervention for severe obesity. NICE recommends considering surgery for adults with a BMI of 40 kg/m² or above, or 35 kg/m² or above with significant obesity-related comorbidities (such as type 2 diabetes or hypertension). For people with recent-onset type 2 diabetes, surgery may be considered at lower BMI thresholds. Ethnicity-adjusted BMI thresholds apply for people from certain ethnic groups. Procedures available through the NHS include gastric bypass, sleeve gastrectomy, and adjustable gastric banding. These interventions typically result in substantial, sustained weight loss and improvement in metabolic conditions.

Patients should consult their GP to discuss which treatment options might be appropriate for their individual circumstances, as eligibility criteria and local commissioning policies may vary across different NHS regions. Further information is available on the NHS website (nhs.uk). If you experience any suspected side effects from obesity medications, you can report them via the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk or through the Yellow Card app.

Clinical Trials and Future Treatment Prospects

The timeline for asprosin-targeted treatments reaching clinical practice remains uncertain, as no human clinical trials of asprosin-blocking therapies have been publicly registered to date (as of early 2025, based on searches of ClinicalTrials.gov, ISRCTN, and the EU Clinical Trials Register). The development pathway for novel obesity medications typically spans 10–15 years from initial discovery to regulatory approval, encompassing preclinical research, Phase I safety studies, Phase II proof-of-concept trials, and large Phase III efficacy studies.

Before asprosin-targeted therapies can enter human testing, several critical questions must be addressed. Researchers need to establish the optimal approach for blocking asprosin activity—whether through monoclonal antibodies, small molecule inhibitors, or other modalities. Safety considerations are paramount: since asprosin plays a physiological role in glucose homeostasis during fasting, blocking its activity might pose risks of hypoglycaemia or other metabolic disturbances, though human safety profiles remain entirely unknown without clinical trial data. Determining the appropriate degree and duration of asprosin inhibition will be essential.

The regulatory pathway in the UK involves rigorous evaluation by the Medicines and Healthcare products Regulatory Agency (MHRA), which assesses safety, quality, and efficacy data before granting marketing authorisation. Following MHRA approval, NICE conducts health technology assessments to determine whether new treatments represent cost-effective use of NHS resources. This process considers clinical effectiveness, quality of life improvements, and economic impact compared to existing therapies.

Realistically, if asprosin-targeted treatments prove successful in early human trials, they would likely first be tested in specific patient populations, such as individuals with severe obesity and metabolic complications who have not responded to existing treatments. The concept of companion diagnostics to measure asprosin levels and identify patients most likely to benefit remains hypothetical at this stage and would require substantial validation.

Other emerging obesity treatments currently in various stages of development include dual GLP-1/GIP receptor agonists. Tirzepatide, for example, has been licensed by the MHRA for weight management (as Mounjaro®), and NICE evaluation is ongoing; patients and clinicians should check the NICE website for the latest guidance on availability through the NHS. Other investigational approaches include amylin analogues and combination therapies targeting multiple metabolic pathways simultaneously.

Patients interested in participating in obesity research can discuss opportunities with their GP or search the NIHR Clinical Research Network portfolio. However, there is no indication that asprosin-targeted treatments will become available in the near future. Anyone struggling with obesity should focus on accessing currently available, evidence-based treatments rather than waiting for experimental therapies. If you have concerns about your weight or metabolic health, contact your GP to discuss appropriate investigation and management options tailored to your individual circumstances.

Frequently Asked Questions

What does asprosin do in the body and how does it relate to obesity?

Asprosin is a hormone released by fat tissue that signals the liver to produce glucose during fasting and may influence appetite in the brain. People with obesity typically have elevated asprosin levels, which are associated with excessive glucose production, insulin resistance, and altered appetite regulation in research studies.

Are there any asprosin-blocking treatments available for obesity right now?

No asprosin-targeted treatments are currently approved or available for clinical use in the UK or elsewhere. Research remains in early laboratory and animal testing stages, with no human clinical trials registered as of 2025.

When can I expect asprosin obesity treatment to become available on the NHS?

The timeline remains highly uncertain, as no human trials have begun and drug development typically takes 10–15 years from discovery to approval. Even if early human trials prove successful, asprosin-targeted treatments would require extensive safety testing, regulatory approval by the MHRA, and cost-effectiveness evaluation by NICE before becoming available through the NHS.

What obesity medications can my GP prescribe instead of waiting for asprosin treatments?

Your GP can discuss several evidence-based options including orlistat (which reduces fat absorption), semaglutide injections (Wegovy), or liraglutide (Saxenda) if you meet specific BMI and health criteria. Eligibility depends on your BMI, ethnicity, existing health conditions, and local NHS commissioning policies, so speak with your GP about which treatments might suit your circumstances.

How do GLP-1 medications like semaglutide compare to potential asprosin treatments?

GLP-1 receptor agonists like semaglutide are proven, MHRA-approved treatments that reduce appetite and slow stomach emptying, with established safety profiles from extensive human trials. Asprosin-targeted therapies remain entirely experimental with unknown human effects, safety profiles, and efficacy, making direct comparison impossible at this stage.

Can I join a clinical trial testing asprosin-blocking drugs for obesity?

No human clinical trials of asprosin-targeted obesity treatments are currently registered or recruiting participants. You can discuss other obesity research opportunities with your GP or search the NIHR Clinical Research Network portfolio, but should focus on accessing currently available evidence-based treatments rather than waiting for experimental therapies.


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The health-related content published on this site is based on credible scientific sources and is periodically reviewed to ensure accuracy and relevance. Although we aim to reflect the most current medical knowledge, the material is meant for general education and awareness only.

The information on this site is not a substitute for professional medical advice. For any health concerns, please speak with a qualified medical professional. By using this information, you acknowledge responsibility for any decisions made and understand we are not liable for any consequences that may result.

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