I'm working on a round-up article for MedCentral on available therapies for MASH with a focus on the MASH pharmacotherapy pipeline. For this, I'm looking for a hepatologist or liver disease specialist to offer expert insights and perspective. Deadline is Tuesday 04/21 EOD. Questions: 1. What are your thoughts on effective available/FDA-approved therapies as well as emerging therapies within the MASH pharmacological landscape? FGF21 analogues 2. How do you see the FGF21 analog class (efruxifermin, pegozafermin, efimosfermin) differentiating itself in MASH, particularly on steatosis, fibrosis, and other metabolic parameters, and which agent currently stands out as the most promising? GLP‑1/GIP‑based agents 3. For GLP‑1/GIP incretin‑based agents (survodutide, tirzepatide, retatrutide, pemvidutide) in MASH, how much of the observed benefit do you think is driven by weight loss versus direct hepatic effects, and what makes one agent stand-out clinically over another in a liver‑focused indication? Lanifibranor, VK2809, belapectin, denifanstat, ervogastat 4. Among lanifibranor, VK2809, belapectin, denifanstat, and ervogastat, which mechanism do you think has the strongest potential to deliver a clinically meaningful MASH benefit, and what are the key gaps in data or safety that still need to be addressed before any of these agents becomes a routine treatment option? 5. Looking ahead, how do you see the MASH pharmacological pipeline evolving over the next 5–10 years, particularly in terms of combination approaches, positioning versus invasive disease endpoints, and which mechanisms can we expect to become first‑line or add‑on therapies?

Hi Oladimeji, I can speak to incretin agents given my experience summarizing clinical use of oral semaglutide (Rybelsus) and its off-label use for weight loss. From that perspective, much of the hepatic benefit seen with GLP-1 and GLP-1/GIP agents is likely driven by weight loss and related metabolic improvements, while any direct liver effects remain under investigation and are not yet clearly separated from weight-driven changes. Therefore, agents with greater weight-loss potency or stronger effects on insulin resistance are more likely to show larger MASH signals; semaglutide is used off-label but obesity-specific formulations often produce larger weight reductions. For a liver-focused indication, evidence of fibrosis improvement independent of weight loss and a safety profile acceptable in patients with advanced liver disease would make an agent stand out, and I can share additional context or examples on request. Best regards, Amir Husen

I stick to addiction recovery and mental health, so I don't know enough about MASH or liver drugs to help here. You should talk to a hepatologist or someone working on those treatments. Whenever I cover topics outside my wheelhouse, I find an expert to interview. A liver doctor will give your readers the right specifics for this article. If you have any questions, feel free to reach out to my personal email

I'm not a liver doctor, but I lead a health tech company so I watch MASH therapies closely. The data we gather at Superpower shows a lot of action in metabolic and inflammatory pathways right now, particularly with FGF21 analogues and GLP-1s. But if you want the real medical answers, you should reach out to a hepatologist running trials. They can give you the details on safety and results from their research and patients, which I can't. If you have any questions, feel free to reach out to my personal email

I focus on integrative general health, so liver disease and MASH drugs are outside my wheelhouse. That area changes so fast that you really need a hepatologist for the specifics. From what I've seen, patients get the best care when I stick to the general stuff and bring in specialists for the complex conditions. You definitely want an expert handling those new MASH treatments to make sure you get it right. If you have any questions, feel free to reach out to my personal email