# Targeted Therapies for Liver Fibrosis in NASH: What Patients Need to Know About Emerging Treatments Nonalcoholic steatohepatitis (NASH) is rapidly becoming the leading cause of cirrhosis and liver transplantation worldwide, yet no drugs are currently approved to treat the liver fibrosis (scarring) it causes. This review examines the most promising experimental and investigational therapies currently in phase 2 and 3 clinical trials, including agents that target metabolic pathways (such as FXR agonists, thyroid hormone receptor beta agonists, FGF-21 analogs, and PPAR agonists) and agents that fight inflammation and fibrosis directly. Key findings include obeticholic acid doubling fibrosis improvement from 11.9% to 23.1%, and semaglutide achieving NASH resolution in up to 59% of patients—though notably without improving fibrosis. The authors express growing optimism that effective pharmacotherapies will emerge within the next 3 years to favorably alter the natural history of this increasingly common disease. # Targeted Therapies for Liver Fibrosis in NASH: What Patients Need to Know About Emerging Treatments ## Table of Contents - Key Points - Background: Why NASH Is Becoming a Major Health Problem - Understanding NASH, Liver Fibrosis, and Cirrhosis - How Liver Fibrosis Is Diagnosed: Moving Beyond Biopsy - About This Review: How the Research Was Conducted - Key Findings: Metabolic Agents for NASH Fibrosis - Key Findings: Anti-Inflammatory and Anti-Fibrotic Agents - Clinical Implications: What This Means for Patients - Limitations: What This Review Could Not Prove - Recommendations for Patients - Frequently Asked Questions - Source Information ## Key Points - No drugs are approved to treat NASH fibrosis; lifestyle change and co-morbidity management remain the foundation of care. - OCA doubled fibrosis improvement from 11.9% to 23.1% in the REGENERATE phase 3 trial, but did not improve NASH resolution. - Semaglutide achieved NASH resolution in up to 59% of patients in a phase 2 trial, yet showed no anti-fibrotic benefit. - Non-invasive tests like FIB-4, transient elastography, and MRI-PDFF are improving, but biopsy is still required for phase 3 approval trials. - Researchers are optimistic that effective pharmacotherapies for NASH fibrosis will be available within the next 3 years. ## Background: Why NASH Is Becoming a Major Health Problem For decades, hepatitis B virus (HBV) and hepatitis C virus (HCV) were the leading causes of cirrhosis and the need for liver transplantation. That picture has changed dramatically. Major advances in antiviral treatment—long-term suppression for HBV and a complete cure for HCV—have dramatically reduced the number of patients progressing to cirrhosis from these viruses. In fact, these treatments have been so effective that they have largely eliminated the need for anti-fibrotic (anti-scarring) therapies in viral hepatitis. However, a new threat has emerged. The prevalence of non-alcoholic fatty liver disease (NAFLD) has been steadily increasing, and a substantial fraction of these patients develop non-alcoholic steatohepatitis (NASH), a more aggressive form of fatty liver disease that can progress to cirrhosis. NASH is now emerging as the leading indication for liver transplantation in North America and Europe. Other causes of cirrhosis include chronic alcohol use, autoimmune hepatitis, primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC). But the importance of treating fibrosis goes beyond end-stage liver disease. Chronic inflammation, fibrosis, and cirrhosis of any cause also significantly increase the risk of hepatocellular carcinoma (HCC), the most common type of primary liver cancer. This is why efforts to prevent fibrosis or promote its regression are critically needed. ## Understanding NASH, Liver Fibrosis, and Cirrhosis Fibrosis—or scarring—is the accumulation of extracellular matrix (ECM) in chronically injured tissues, including the liver. In NASH, fibrosis is the key determinant of clinical outcomes. The more scarring, the worse the prognosis. The process begins with damage to hepatocytes (liver cells). This damage provokes inflammation, secretion of cytokines (cell-signaling proteins), and hepatocyte apoptosis (programmed cell death). These and other convergent drivers lead to the activation of hepatic stellate cells (HSCs), a type of resident liver cell that is the primary source of ECM accumulation. In simple terms, when liver cells are injured, stellate cells go into overdrive and produce scar tissue. Several circulating cytokines, mediators, and growth factors are implicated in this scarring process, including: - **TGFβ1** (transforming growth factor beta 1), a key pro-fibrotic signal - **Metalloproteinases**, enzymes that remodel the ECM - **PDGF** (platelet-derived growth factor) - **VEGF** (vascular endothelial growth factor) Within both hepatocytes and stellate cells, intracellular signaling networks attempt to restore normal liver balance. These include nuclear receptors such as FXR (farnesoid X receptor), PPAR (peroxisome proliferator-activated receptor), and the vitamin D receptor. However, signals from damaged or dying hepatocytes can directly provoke stellate cell activation, creating a vicious cycle. Additional triggers for stellate cell activation include the direct toxic effects of free cholesterol and increased levels of insulin. The good news is that each step in this cascade of liver injury and fibrosis represents a potential target for anti-fibrotic therapies—and many of these targets are now being actively tested in clinical trials. ## How Liver Fibrosis Is Diagnosed: Moving Beyond Biopsy Traditionally, liver biopsy has been the "gold standard" for diagnosing fibrosis. However, that status is being reconsidered. Biopsy is prone to sampling variability—meaning the needle might miss areas of significant scarring—and cannot be performed more than 2–3 times during the course of a clinical trial. It is also invasive and not without risks. Fortunately, non-invasive methods of diagnosis are urgently needed and rapidly developing. Blood tests widely used include: - **The ELF test** (Enhanced Liver Fibrosis test) - **The NAFLD fibrosis score** - **The Fibrosis-4 (FIB-4) Index**, which incorporates the patient's age, ALT (alanine aminotransferase), AST (aspartate aminotransferase), and platelet count. FIB-4 has a high negative predictive value for excluding advanced fibrosis—meaning if the score is low, advanced fibrosis is unlikely. Imaging-based approaches are also advancing. **Transient elastography (TE)**, which uses a bedside device to assess liver stiffness, has high sensitivity but is less accurate in obese patients. **MR elastography** offers higher specificity than TE and can help rule out fibrosis. **Corrected T1 imaging** is another emerging modality. **MRI-PDFF** (magnetic resonance imaging proton density fat fraction) shows great promise as a way to assess liver fat content. These non-invasive tools are urgently needed because they are objective and reduce the need for invasive procedures. However, they are not yet sufficiently validated to replace liver biopsy in Phase 3 clinical trials seeking regulatory approval—which is why many of the trials described below still rely on biopsy to measure treatment response. ## About This Review: How the Research Was Conducted This article is a review paper, not a clinical trial itself. The authors—researchers from the Division of Liver Diseases at the Icahn School of Medicine at Mount Sinai in New York—systematically reviewed the current state of research on experimental and investigational therapies for NASH fibrosis. They focused on drugs in phase 2 and phase 3 clinical trials, organizing the candidates by their mechanism of action. The review covers agents that target metabolic processes in the liver separately from agents that target inflammation and fibrosis directly, and it highlights the diagnostic methods used in each study. The goal was to synthesize the latest evidence on which therapies are most likely to reach patients in the near future. ## Key Findings: Metabolic Agents for NASH Fibrosis At present, there are **no drugs approved** to specifically treat hepatic fibrosis in NASH or any chronic liver disease. However, many promising candidates are in development. Interestingly, effective antiviral therapy in HBV and HCV has a significant anti-fibrotic impact simply by restoring hepatocellular health and promoting fibrosis regression. This tells us that the healing liver has built-in anti-fibrotic pathways—and that therapeutic strategies to reverse fibrosis are achievable. ### FXR Agonists: Reviving a Key Nuclear Receptor The nuclear receptor FXR regulates many intracellular pathways, including cholesterol metabolism, and is downregulated during the development of fibrosis. Several FXR agonists are in clinical development, led by **obeticholic acid (OCA)**. OCA has been studied in phase 2 and phase 3 clinical trials. In the phase 3 **REGENERATE** trial (NCT02548351), OCA **doubled the percentage of patients who had reduced fibrosis, from 11.9% to 23.1%**. However, it did not statistically improve the likelihood of resolution of NASH, and it has not yet been approved for NASH. Notably, OCA is already approved and effective in primary biliary cholangitis, where it significantly delays disease progression. An ongoing phase 3 trial called **REVERSE** (NCT03439254) is studying OCA specifically in cirrhotic patients with NASH. This double-blind, randomized, placebo-controlled trial is seeking evidence of fibrosis improvement in this more advanced patient population. Other FXR agonists in development include: - **EDP-305**, in a phase 2 randomized, double-blind, placebo-controlled study (NCT03421431), evaluating its ability to reduce ALT in patients with biopsy-proven NASH. - **Tropifexor**, being evaluated in combination with **cenicriviroc** (which blocks the chemokine receptors CCR2 and CCR5) in the TANDEM trial (NCT03548444). - **Cilofexor**, another FXR agonist under evaluation in combination therapy. Additionally, **clesacostat (PF-05221304)** blocks the enzymes acetyl CoA carboxylase 1 and 2, which reduces liver fat content and is being studied in a phase 2 trial (NCT03248882). ### Thyroid Hormone Receptor Beta (THR-β) Agonists Selective agonism of thyroid beta receptors (THR-β) is attracting significant interest. This mechanism has the relative advantage of improving cardiovascular risk factors while potentially attenuating the severity of NASH. The **MAESTRO-NASH** trial (NCT03900429) is a double-blind, placebo-controlled, randomized phase 3 trial testing **Resmetirom (MGL-3196)**, a THR-β agonist thought to improve NASH by increasing hepatic fat metabolism. The primary endpoint is biopsy-proven resolution of NASH in non-cirrhotic patients with stage 2 or 3 fibrosis. **VK 2809**, another drug in this class, is being studied in a phase 2 trial (NCT02927184) in patients with NAFLD and primary hypercholesterolemia. That study measures changes in LDL-C (bad cholesterol) as a primary outcome, with reduction in liver fat on MRI-PDFF as a secondary outcome. Other THR-β agonists are also in development. ### FGF-21 Analogues: Targeting Metabolism and Fibrosis FGF-21 (fibroblast growth factor 21) analogues are being developed by multiple companies because of their ability to improve glucose homeostasis and insulin sensitivity, in addition to potential anti-fibrotic activity. **Pegbelfermin** (also known as PEG-FGF21), a pegylated FGF-21, has been tested in a multicenter, randomized, double-blind, placebo-controlled phase 2 study. The trial included patients with a BMI greater than 25, biopsy-proven NASH with fibrosis stage 1–3, and an MRI-PDFF score of at least 10%. Patients received either placebo, 10 mg, or 20 mg of pegbelfermin. The results were striking. The drug produced a significant improvement in MRI-PDFF absolute fat fraction compared to placebo: - In the **10 mg group**: −6.8% versus −1.3% for placebo (**p=0.0004**) - In the **20 mg group**: −5.2% versus −1.3% for placebo (**p=0.008**) A phase 3 trial is expected to follow to further assess liver histology and safety. Pegbelfermin is additionally being evaluated in the **FALCON 2** study, a phase 2 randomized, double-blind, placebo-controlled study in patients with NASH or compensated cirrhosis, with the primary outcome being a reduction of at least 1 stage of fibrosis on biopsy. The **FALCON 1** study is a phase 2B trial looking at patients with NASH and stage 3 fibrosis, with the same primary endpoint. Other FGF-21 agents include: - **BIO89-100**, which has a different structure than pegbelfermin, currently in a phase 2 randomized, double-blind, placebo-controlled study (NCT04048135) focusing on patients with steatosis on fibroscan or MRI-PDFF, as well as biopsy-proven NASH with central obesity, diabetes, or elevated ALT. - **Efruxifermin**, a third FGF-21 agent in a phase 2 randomized, double-blind, placebo-controlled study (NCT03976401) seeking reduction in fat on MRI-PDFF in patients with biopsy-proven NASH. ### FGF19-Based Therapies FGF19 is a fibroblast growth factor that promotes hepatocyte proliferation but also has anti-fibrotic and beneficial metabolic activity. To eliminate the risk of carcinogenesis (cancer formation), the parent molecule was engineered to remove its growth-promoting activity while preserving its beneficial metabolic effects. The resulting molecule, **aldafermin**, showed striking anti-fibrotic activity within 4 months in a phase 2 trial. A related approach uses an antibody to activate the FGF19 receptor (FGFR1/β-Klotho), which has shown promise in animal studies and is now being evaluated in a phase 2 study seeking histologic resolution of NASH as the primary endpoint (NCT04171765). ### PPAR Agonists: Regulating Cholesterol and Lipid Metabolism The peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that regulate cholesterol metabolism and dyslipidemia. There are three subgroups: - **PPARα**: involved in ketogenesis (production of ketone bodies) - **PPARγ**: involved in lipid uptake - **PPARδ**: involved in the catabolism (breakdown) of cholesterol The **EVIDENCES IV** trial (NCT03061721) is a phase 2 study of **Saroglitazar**, a PPAR α/γ agonist, powered to demonstrate a reduction in ALT in NASH/NAFLD patients diagnosed by either biopsy or imaging. **Lanifibranor**, a PPARα/γ/δ agonist (NCT03008070), is being evaluated in a biopsy-based phase 2 study known as the NATIVE trial, assessing response in the SAF (Steatosis, Activity, Fibrosis) score, defined as a decrease of at least 2 points. **Seladelpar**, a PPAR δ agonist (NCT03551522), is in a phase 2 trial using MRI-PDFF to assess reduction in hepatic fat content. Tragically, one notable failure occurred: **RESOLVE-IT**, a phase 3 study using **Elafibranor**, a PPAR α/δ agonist, evaluated patients with NASH seeking histological improvement. The primary endpoint was **not met**, underscoring the difficulty of translating promising early results into late-stage success. ### GLP-1 Receptor Agonists: A Surprising Finding A growing list of drugs focuses on improving glucose homeostasis as a means to improve NASH. The most prominent of these is **Semaglutide**, a GLP-1R (glucagon-like peptide-1 receptor) agonist that promotes insulin secretion from pancreatic beta cells. In a phase 2 double-blind, randomized trial (NCT02970942), 320 patients with biopsy-confirmed NASH and liver fibrosis (stage 1–3) received either placebo, 0.1 mg, 0.2 mg, or 0.4 mg of semaglutide. The primary endpoint was NASH resolution without worsening of fibrosis, and a secondary endpoint was improvement in fibrosis stage in patients with stage 2 or 3 disease. The results showed a statistically significant, dose-dependent response in NASH resolution: 1. **Placebo group**: 17% of patients achieved NASH resolution 1. **0.1 mg group**: 40% of patients achieved NASH resolution 1. **0.2 mg group**: 36% of patients achieved NASH resolution 1. **0.4 mg group**: 59% of patients achieved NASH resolution (**P<0.001** versus placebo) Surprisingly, despite this dramatic benefit in NASH resolution, there was **no anti-fibrotic activity** observed (the secondary outcome). This tells researchers that resolving the inflammation of NASH does not automatically reverse established scar tissue. A larger phase 3 study is anticipated. ### Other Metabolic Approaches Several other metabolic agents are in earlier stages of investigation: - **Aldosterone receptor antagonist** (NCT02923154): phase 2 study measuring ALT levels as a surrogate for treatment response. - **HTD1801** (NCT03656744): a lipid modulator being tested in phase 2 in patients with NASH and diabetes mellitus, measuring decrease in fat content on MRI-PDFF as a primary outcome. - **PXL 770** (NCT03763877): activates AMPK (adenosine monophosphate-activated protein kinase), which regulates cellular response to ischemia, stress, and energy deprivation. This phase 2 study measures improvement in liver fat by MRI-PDFF. - **TVB-2640** (NCT03938246): a FASN (fatty acid synthase) inhibitor—an essential enzyme in de-novo synthesis of long-chain fatty acids—using MRI-PDFF to measure reduction in hepatic fat. - **Elobixibat** (NCT04006145): an IBAT (ileal bile acid transporter) inhibitor, measuring change in serum LDL-C as a primary outcome, with fibrosis measured via surrogates such as the Fibrosis-4 Index. - **MSDC-0602K** (NCT02784444): a MPC (mitochondrial pyruvate carrier) modulator involved in fat metabolism, in a phase 2 trial with a primary endpoint of at least a 2-point improvement on the NAS (NAFLD Activity Score) in patients with NASH fibrosis. - **Icosabutate** (NCT04052516): a structurally engineered fatty acid thought to have anti-fibrotic effects, increase insulin sensitivity, and decrease hepatic lipotoxicity (fat-induced liver damage). A recent mouse study showed decreased hepatic fibrosis, lower lipid levels, increased lipid metabolism in the liver, and downregulated inflammatory pathways. The phase 2 trial uses histologic confirmation of NASH resolution without worsening of fibrosis as the primary endpoint, with improvement in the NAFLD activity score as a secondary endpoint. ## Key Findings: Anti-Inflammatory and Anti-Fibrotic Agents While metabolic agents aim to fix the underlying liver injury, a separate class of drugs targets inflammation and fibrosis more directly. **SSAO**, better known as **VAP-1** (Vascular Adhesion Protein-1), is an enzyme that promotes inflammation in the liver with subsequent fibrosis. It is increased in patients with chronic liver disease. The SSAO-inhibitor **BI 1467335** is being studied in a phase 2 trial (NCT03166735), measuring reduction in the levels of the biomarker amine oxidase copper-containing 3 as a primary outcome. Secondary outcomes include reduction in ALT, AST, alkaline phosphatase, and gamma-glutamyl transferase (GGT). **Hepastem** are liver-derived mesenchymal stem cells proposed to decrease inflammation, deactivate hepatic stellate cells, and thereby reduce fibrosis. NCT03963921 is an open-label, multi-center study focused on safety and tolerability in patients with fibrosis or cirrhosis on histology. **Natural Killer (NK) cells** are generally protective against infection and inflammation. However, in patients with liver fibrosis, they may become dysfunctional, worsening liver injury and inflammation. An NK cell antagonist, **GRI0621**, is being tested in a double-blind, randomized, placebo-controlled phase 2 study (NCT02949375) using ALT as a marker of response to treatment in patients with NASH. ## Clinical Implications: What This Means for Patients There are currently **no approved pharmaceutical treatments** for NASH fibrosis. Lifestyle modifications and treatment of underlying co-morbidities—such as obesity, diabetes, and high cholesterol—remain the mainstay of treatment for NASH and its associated fibrosis. However, the landscape is shifting rapidly. The authors of this review highlight several reasons for optimism: - Multiple phase 3 trials are now underway for leading candidates, including OCA, resmetirom, and semaglutide. - The success of antiviral therapies in reversing fibrosis in hepatitis B and C proves that the liver has endogenous (built-in) anti-fibrotic pathways that can be harnessed. - Non-invasive markers of fibrosis are improving, which will accelerate clinical trial evaluation and eventually allow more patients to be monitored without repeated biopsies. - Combination therapies (for example, an FXR agonist plus a CCR2/CCR5 antagonist) are being explored, recognizing that NASH fibrosis involves multiple pathways. The authors state: "While no drugs are approved yet for NASH fibrosis, there is growing optimism that new pharmacotherapies are likely to emerge within the next 3 years that will favorably alter the natural history of disease." This matters for patients because fibrosis is the key driver of clinical outcomes in NASH. Successfully treating fibrosis could reduce the risk of progression to cirrhosis, liver failure, and hepatocellular carcinoma (HCC), and ultimately reduce the need for liver transplantation. ## Limitations: What This Review Could Not Prove Several important limitations must be considered when interpreting these findings: - **Liver biopsy remains the standard for regulatory approval**, but it is imperfect. The authors note that biopsy is "prone to sampling variability and cannot be performed more than 2–3 times during the course of a clinical trial." - **Non-invasive markers are not yet validated enough** to replace biopsy in Phase 3 clinical trials seeking regulatory approval, although they are rapidly improving. - **Transient elastography is less accurate in obese patients**—a significant limitation given that obesity is a major driver of NASH. - **Many of the reviewed therapies are still in phase 2 trials**, meaning their efficacy and safety are not yet confirmed by large-scale, late-stage studies. - **Drugs may not be directly anti-fibrotic**. Several agents being tested for NASH fibrosis may improve fibrosis only by attenuating the upstream cellular injury and metabolic drivers of fibrogenesis. Semaglutide is a clear example: it dramatically improved NASH resolution but showed no direct anti-fibrotic benefit. - **Histological improvement does not always translate to clinical benefit**—the field still needs to demonstrate that these drugs reduce hard outcomes like progression to cirrhosis, decompensation, need for transplantation, and death. - The phase 3 trial for elafibranor (RESOLVE-IT) failed to meet its primary endpoint, a reminder that many promising agents will not ultimately succeed. ## Recommendations for Patients For patients living with NASH or NAFLD, this review offers several practical takeaways: 1. **Lifestyle modification is still the foundation of care.** Weight loss, dietary changes, and exercise remain the most proven approaches to improving NASH and its associated fibrosis. No drug can replace these measures. 1. **Manage co-morbidities aggressively.** The review emphasizes that treating underlying conditions—including obesity, type 2 diabetes, and dyslipidemia (abnormal cholesterol)—is the mainstay of current medical care for NASH. 1. **Ask about non-invasive monitoring.** If you have NAFLD or NASH, discuss blood-based tests like the FIB-4 index or NAFLD fibrosis score, or imaging like transient elastography or MRI-PDFF with your hepatologist. These tools are becoming more accurate and may reduce the need for repeated biopsies. 1. **Consider clinical trials.** For patients with biopsy-proven NASH and fibrosis, participation in clinical trials offers access to promising investigational therapies. The "next 3 years" window highlighted by the authors suggests that trial results will be arriving soon. 1. **Be patient but proactive.** The science of anti-fibrotic therapy for NASH is advancing rapidly, but regulatory approval takes time. Work with a liver specialist (hepatologist) who can help you navigate emerging treatment options and determine if you might be a candidate for investigational therapies. ## Frequently Asked Questions ### What is NASH fibrosis and why does it matter? NASH is an aggressive form of fatty liver disease that can cause liver fibrosis, or scarring. Fibrosis is the key driver of clinical outcomes in NASH—the more scarring, the worse the prognosis. Advanced fibrosis can progress to cirrhosis, liver failure, and liver cancer, so treating fibrosis is critically important. ### Are there any approved drugs to treat NASH fibrosis? No drugs are currently approved specifically to treat liver fibrosis in NASH. Lifestyle modification and treatment of co-morbidities like obesity, diabetes, and high cholesterol remain the mainstays of care. However, multiple phase 2 and phase 3 trials are testing promising investigational therapies, and researchers are optimistic that new pharmacotherapies will emerge within the next 3 years. ### What were the key results with obeticholic acid (OCA) for NASH fibrosis? In the phase 3 REGENERATE trial, obeticholic acid doubled the percentage of patients who had reduced fibrosis, from 11.9% to 23.1%. However, it did not statistically improve the likelihood of NASH resolution. OCA is already approved for primary biliary cholangitis, and an ongoing phase 3 trial called REVERSE is studying it in cirrhotic NASH patients. ### How well did semaglutide work for NASH? In a phase 2 trial of 320 patients with biopsy-confirmed NASH and fibrosis, semaglutide led to NASH resolution in up to 59% of patients taking the highest dose, compared with 17% on placebo. However, surprisingly, there was no improvement in fibrosis. This shows that resolving NASH inflammation does not automatically reverse established scar tissue. ### What is the FIB-4 index and how is it used? The Fibrosis-4 (FIB-4) Index is a blood test that incorporates your age, ALT, AST, and platelet count. It has a high negative predictive value for excluding advanced fibrosis—meaning if the score is low, advanced fibrosis is unlikely. It is one of several non-invasive tools being used to monitor liver fibrosis and may reduce the need for repeated biopsies. ### Can lifestyle changes really help NASH fibrosis? Yes. The review states that lifestyle modification and treatment of underlying co-morbidities—such as obesity, diabetes, and high cholesterol—remain the mainstay of treatment for NASH and its associated fibrosis. Weight loss, dietary changes, and exercise are the most proven approaches. No drug can replace these measures at this time. ### Should I consider joining a clinical trial for NASH fibrosis? For patients with biopsy-proven NASH and fibrosis, participation in clinical trials offers access to promising investigational therapies. The review notes that trial results are expected within the next 3 years. Talk to a liver specialist about whether you might be a candidate, and ask about non-invasive monitoring options to reduce the need for repeated biopsies. ### Can a second opinion change my treatment plan for NASH-related liver fibrosis? Because no drugs are approved to treat NASH fibrosis, treatment plans rely on lifestyle changes, managing diabetes and cholesterol, and possibly clinical trials. A second opinion can help confirm whether a biopsy was read correctly, since biopsy can miss areas of scarring. It can also clarify whether non-invasive tests such as FIB-4 or elastography are appropriate for monitoring, and whether an investigational therapy—like an FXR agonist or THR-β agonist—might be a reasonable option. Diagnostic Detectives Network provides independent expert second opinions. ## Source Information **Original article title:** Targeted Therapies for the Management of Fibrosis in NASH **Authors:** Tsipora M Huisman, Douglas T Dieterich, and Scott L Friedman **Affiliation:** Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA **Journal:** Journal of Experimental Pharmacology, 2021:13, pages 329–338 **DOI** --- Publisher: Diagnostic Detectives Network (https://diagnosticdetectives.com) — independent multi-expert medical second opinions, worldwide, private-pay. Author byline: Anton Titov, MD, PhD. Contact: https://diagnosticdetectives.com/pages/contact Canonical page: https://diagnosticdetectives.com/products/targeted-therapies-for-liver-fibrosis-in-nash-what-patients-need-to-know-about-emerging-treatments