Journal articles: 'Antifibrotic Agents'

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Albanis, E., and S. L. Friedman. "Antifibrotic Agents for Liver Disease." American Journal of Transplantation 6, no. 1 (January 2006): 12–19. http://dx.doi.org/10.1111/j.1600-6143.2005.01143.x.

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LaCamera, Peter P., Susan L. Limb, Tmirah Haselkorn, Elizabeth A. Morgenthien, John L. Stauffer, and Mark L. Wencel. "Physician characteristics associated with treatment initiation patterns in idiopathic pulmonary fibrosis." Chronic Respiratory Disease 16 (January 1, 2019): 147997311987967. http://dx.doi.org/10.1177/1479973119879678.

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Pirfenidone and nintedanib are oral antifibrotic agents approved for the treatment of idiopathic pulmonary fibrosis (IPF). Real-world data on factors that influence IPF treatment decisions are limited. Physician characteristics associated with antifibrotic therapy initiation following an IPF diagnosis were examined in a sample of US pulmonologists. An online, self-administered survey was fielded to pulmonologists between April 10, 2017, and May 17, 2017. Pulmonologists were included if they spent >20% of their time in direct patient care and had ≥5 patients with IPF receiving antifibrotics. Participants answered questions regarding timing and reasons for considering the initiation of antifibrotic therapy after an IPF diagnosis. A total of 169 pulmonologists participated. The majority (81.7%) considered initiating antifibrotic therapy immediately after IPF diagnosis all or most of the time (immediate group), while 18.3% considered it only some of the time or not at all (delayed group). Pulmonologists in the immediate group were more likely to work in private practice (26.1%), have a greater mean percentage of patients receiving antifibrotic therapy (60.8%), and decide to initiate treatment themselves (31.2%) versus those in the delayed group (16.1%, 30.5%, and 16.1%, respectively). Most pulmonologists consider initiating antifibrotic treatment immediately after establishing an IPF diagnosis all or most of the time versus using a “watch-and-wait” approach. Distinguishing characteristics between pulmonologists in the immediate group versus the delayed group included practice setting, percentage of patients receiving antifibrotic therapy, and the decision-making dynamics between the patient and the pulmonologist.

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Skuta, Gregory L. "Antifibrotic Agents in Glaucoma Filtering Surgery." International Ophthalmology Clinics 33, no. 4 (1993): 165–82. http://dx.doi.org/10.1097/00004397-199303340-00014.

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Oishi, Keiji, Tsunahiko Hirano, Yoriyuki Murata, Kazuki Hamada, Sho Uehara, Ryo Suetake, Yoshikazu Yamaji, et al. "Medication persistence rates and predictive factors for discontinuation of antifibrotic agents in patients with idiopathic pulmonary fibrosis: a real-world observational study." Therapeutic Advances in Respiratory Disease 13 (January 2019): 175346661987289. http://dx.doi.org/10.1177/1753466619872890.

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Background: In patients with idiopathic pulmonary fibrosis (IPF), continuing treatment with antifibrotic agents is crucial to decrease the reduction of forced vital capacity and mortality rate. However, predictive factors for the discontinuation of antifibrotic agents are unknown. This study aims to investigate the clinical characteristics and predictive factors for the discontinuation of antifibrotic agents in patients with IPF. Methods: This was a double-center retrospective study that enrolled patients with IPF treated with pirfenidone or nintedanib between 2009 and 2017. We compared clinical parameters between the medication-continuing group and the discontinued group. The predictive factors were determined using Cox proportional hazards analyses. Results: A total of 66 subjects were included: 43 received pirfenidone and 23 received nintedanib. At 1 year, 23 of 66 patients had discontinued due to adverse events ( n = 12), disease progression ( n = 9), or death ( n = 2). The characteristics of the discontinuation group were poor performance status (PS) and delay from diagnosis to treatment. In the receiver operating characteristic (ROC) analysis associated with the discontinuation of antifibrotic agents, PS was the highest area under the ROC curve (AUC) value (cut-off value, 2; AUC, 0.83; specificity, 63%; sensitivity, 87%). This finding was consistent even when analyzing, except for examples of death and adjusting for the type of antifibrotic agent. The treatment persistence rate by PS was PS 0–1 = 90%, PS 2 = 65%, and PS 3 = 19%. Analysis of the relationship between PS and administration period of antifibrotic agents revealed that delays from diagnosis to treatment led to worsening of dyspnea, a decline in lung function, and deterioration of PS. Conclusions: PS may be informative for predicting discontinuation of medication. Our data reinforced the importance of early initiation of antifibrotic treatment, and we suggest PS should be used as a guide for starting antifibrotic agents in everyday practice. The reviews of this paper are available via the supplementary material section.

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Kawada, Norifumi. "Antifibrotic agents emerging from traditional herbal medicine." Arab Journal of Gastroenterology 10, no. 4 (April 2010): S21—S22. http://dx.doi.org/10.1016/j.ajg.2009.12.007.

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Geismar, Lois S., Janet S. Kerr, Robert L. Trelstad, and David J. Riley. "Treatment of experimental silicosis with antifibrotic agents." Toxicology 53, no. 2-3 (December 1988): 331–44. http://dx.doi.org/10.1016/0300-483x(88)90225-9.

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Grotendorst, Gary R. "Identification and development of novel antifibrotic agents." Expert Opinion on Investigational Drugs 6, no. 6 (June 1997): 777–81. http://dx.doi.org/10.1517/13543784.6.6.777.

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Jegal, Yangjin, Jong Sun Park, Song Yee Kim, Hongseok Yoo, Sung Hwan Jeong, Jin Woo Song, Jae Ha Lee, et al. "Clinical Features, Diagnosis, Management, and Outcomes of Idiopathic Pulmonary Fibrosis in Korea: Analysis of the Korea IPF Cohort (KICO) Registry." Tuberculosis and Respiratory Diseases 85, no. 2 (April 1, 2022): 185–94. http://dx.doi.org/10.4046/trd.2021.0123.

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Background: The Korea Interstitial Lung Disease Study Group has made a new nationwide idiopathic pulmonary fibrosis (IPF) registry because the routine clinical practice has changed due to new guidelines and newly developed antifibrotic agents in the recent decade. The aim of this study was to describe recent clinical characteristics of Korean IPF patients.Methods: Both newly diagnosed and following IPF patients diagnosed after the previous registry in 2008 were enrolled. Survival analysis was only conducted for patients diagnosed with IPF after 2016 because antifibrotic agents started to be covered by medical insurance of Korea in October 2015.Results: A total of 2,139 patients were analyzed. Their mean age at diagnosis was 67.4±9.3 years. Of these patients, 76.1% were males, 71.0% were ever-smokers, 14.4% were asymptomatic at the time of diagnosis, and 56.9% were at gender-agephysiology stage I. Occupational toxic material exposure was reported in 534 patients. The mean forced vital capacity was 74.6% and the diffusing capacity for carbon monoxide was 63.6%. Treatment with pirfenidone was increased over time: 62.4% of IPF patients were treated with pirfenidone initially. And 79.2% of patients were treated with antifiboritics for more than three months during the course of the disease since 2016. Old age, acute exacerbation, treatment without antifibrotics, and exposure to wood and stone dust were associated with higher mortality.Conclusion: In the recent Korean IPF registry, the percentage of IPF patients treated with antifibrotics was increased compared to that in the previous IPF registry. Old age, acute exacerbation, treatment without antifibrotics, and exposure to wood and stone dust were associated with higher mortality.

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Schuppan, Detlef, Muhammad Ashfaq-Khan, Ai Ting Yang, and Yong Ook Kim. "Liver fibrosis: Direct antifibrotic agents and targeted therapies." Matrix Biology 68-69 (August 2018): 435–51. http://dx.doi.org/10.1016/j.matbio.2018.04.006.

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Pan, Xiaoqi, Xiao Ma, Yinxiao Jiang, Jianxia Wen, Lian Yang, Dayi Chen, Xiaoyu Cao, and Cheng Peng. "A Comprehensive Review of Natural Products against Liver Fibrosis: Flavonoids, Quinones, Lignans, Phenols, and Acids." Evidence-Based Complementary and Alternative Medicine 2020 (October 5, 2020): 1–19. http://dx.doi.org/10.1155/2020/7171498.

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Liver fibrosis resulting from continuous long-term hepatic damage represents a heavy burden worldwide. Liver fibrosis is recognized as a complicated pathogenic mechanism with extracellular matrix (ECM) accumulation and hepatic stellate cell (HSC) activation. A series of drugs demonstrate significant antifibrotic activity in vitro and in vivo. No specific agents with ideally clinical efficacy for liver fibrosis treatment have been developed. In this review, we summarized the antifibrotic effects and molecular mechanisms of 29 kinds of common natural products. The mechanism of these compounds is correlated with anti-inflammatory, antiapoptotic, and antifibrotic activities. Moreover, parenchymal hepatic cell survival, HSC deactivation, and ECM degradation by interfering with multiple targets and signaling pathways are also involved in the antifibrotic effects of these compounds. However, there remain two bottlenecks for clinical breakthroughs. The low bioavailability of natural products should be improved, and the combined application of two or more compounds should be investigated for more prominent pharmacological effects. In summary, exploration on natural products against liver fibrosis is becoming increasingly extensive. Therefore, natural products are potential resources for the development of agents to treat liver fibrosis.

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Ismail, Magda M. F., and Eman Noaman. "Novel Pirfenidone Analogs as Antifibrotic Agents: Synthesis and Antifibrotic Evaluation of 2-Pyridones and Fused Pyridones." Medicinal Chemistry Research 14, no. 7 (October 2005): 382–403. http://dx.doi.org/10.1007/s00044-006-0146-2.

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Slabaugh, Mark, and Sarwat Salim. "Use of Anti-VEGF Agents in Glaucoma Surgery." Journal of Ophthalmology 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/1645269.

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A number of antivascular endothelial growth factor agents are currently available to treat various ocular conditions. These agents have similar, but distinct, biologic qualities and have been explored in the management of neovascular glaucoma and in glaucoma surgery. Several different delivery methods are described, and because these medications are routinely given as intraocular injections, some benefits over traditional antifibrotic medications when used in glaucoma surgery are noted. These agents effectively induce regression of anterior segment neovascularization and facilitate initial surgical management of neovascular glaucoma, but the long-term outcome of this condition remains dependent on definitive management of the underlying process. Use in trabeculectomy or tube shunt procedures for other types of glaucoma has shown promise in modulating bleb morphology but has not yet been found to be as effective as traditional antifibrotic agents. There are reports of persistently raised intraocular pressure after repeated use of the anti-VEGF agents, possibly related to frequency of injection. These medications have wide application in the field of surgical glaucoma, but a definitive role has yet to be defined.

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Fitzgerald, L. J., D. N. O'Dwyer, E. Wakeam, D. M. Lyu, and M. P. Combs. "Evaluation of Pre-Transplant Antifibrotic Agents on Post-Transplant Outcomes." Journal of Heart and Lung Transplantation 41, no. 4 (April 2022): S422—S423. http://dx.doi.org/10.1016/j.healun.2022.01.1064.

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Selman, Moisés. "From Anti-inflammatory Drugs Through Antifibrotic Agents to Lung Transplantation." Chest 122, no. 3 (September 2002): 759–61. http://dx.doi.org/10.1378/chest.122.3.759.

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Mannem, Hannah, and Alexander Sasha Krupnick. "Commentary: Antifibrotic agents in the postoperative period: Friends or foes?" Journal of Thoracic and Cardiovascular Surgery 158, no. 1 (July 2019): 297–98. http://dx.doi.org/10.1016/j.jtcvs.2019.02.102.

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Takehara, Kazutaka, Yasuhiko Koga, Yoshimasa Hachisu, Mitsuyoshi Utsugi, Yuri Sawada, Yasuyuki Saito, Seishi Yoshimi, et al. "Differential Discontinuation Profiles between Pirfenidone and Nintedanib in Patients with Idiopathic Pulmonary Fibrosis." Cells 11, no. 1 (January 2, 2022): 143. http://dx.doi.org/10.3390/cells11010143.

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Antifibrotic agents have been widely used in patients with idiopathic pulmonary fibrosis (IPF). Long-term continuation of antifibrotic therapy is required for IPF treatment to prevent disease progression. However, antifibrotic treatment has considerable adverse events, and the continuation of treatment is uncertain in many cases. Therefore, we examined and compared the continuity of treatment between pirfenidone and nintedanib in patients with IPF. We retrospectively enrolled 261 consecutive IPF patients who received antifibrotic treatment from six core facilities in Gunma Prefecture from 2009 to 2018. Among them, 77 patients were excluded if the antifibrotic agent was switched or if the observation period was less than a year. In this study, 134 patients treated with pirfenidone and 50 treated with nintedanib were analyzed. There was no significant difference in patient background, discontinuation rate of antifibrotic treatment over time, and survival rate between the two groups. However, the discontinuation rate due to adverse events within one year of antifibrotic treatment was significantly higher in the nintedanib group than in the pirfenidone group (76% vs. 37%, p < 0.001). Furthermore, the discontinuation rate due to adverse events in nintedanib was higher than that of pirfenidone treatment throughout the observation period (70.6% vs. 31.2%, p = 0.016). The pirfenidone group tended to be discontinued due to acute exacerbation or transfer to another facility. The results of this study suggest that better management of adverse events with nintedanib leads to more continuous treatment that prevents disease progression and acute exacerbations, thus improving prognosis in patients with IPF.

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Hassanein, Tarek, Dean Tai, Chenghai Liu, Terry D. Box, Myron J. Tong, Lorenzo Rossaro, Renee Pozza, et al. "Efficacy and Safety of a Botanical Formula Fuzheng Huayu for Hepatic Fibrosis in Patients with CHC: Results of a Phase 2 Clinical Trial." Evidence-Based Complementary and Alternative Medicine 2022 (July 15, 2022): 1–11. http://dx.doi.org/10.1155/2022/4494099.

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Background. Hepatitis C virus (HCV) is a common cause of progressive hepatic fibrosis, cirrhosis, and hepatocellular carcinoma worldwide. Despite the availability of effective direct-acting antivirals, patients often have significant hepatic fibrosis at the time of diagnosis due to delay in diagnosis and comorbidities which promote fibrogenesis. Thus, antifibrotic agents represent an attractive adjunctive therapy. Fuzheng Huayu (FZHY), a traditional Chinese medicine botanical formulation, has been used as an antifibrotic agent in chronic HBV infection. Our aim was to assess FZHY in patients with HCV infection and active viremia. Method. We randomized 118 patients with active viremia from 8 liver centers in the U.S. to receive oral FZHY (n = 59) or placebo (n = 59) for 48 weeks. Efficacy was assessed by histopathologic changes at the end of therapy. A subset of biopsies was further analyzed using qFibrosis to detect subtle changes in fibrosis in different zones of the hepatic lobules. Results. FZHY was well tolerated and safe. Patients with baseline Ishak fibrosis stages F3 and F4 had better response rates to FZHY than patients with baseline F0–F2 ( p = 0.03 ). qFibrosis zonal analysis showed significant improvement in fibrosis in all zones in patients with regression of the fibrosis stage. Conclusions. FZHY produced antifibrotic effects in patients with baseline Ishak F3 and F4 fibrosis stages. Reduction in fibrosis severity was zonal and correlated with the severity of inflammation. Based on its tolerability, safety, and efficacy, FZHY should be further investigated as a therapy in chronic liver diseases because of its dual anti-inflammatory and antiibrotic properties. Lay Summary. This is the first US-based, multicenter and placebo-controlled clinical trial that shows statistically significant reduction in fibrosis in patients with active HCV using an antifibrotic botanical formula. This has important implications as there is an immediate need for effective antifibrotic agents in treating many chronic diseases including NASH that lead to scarring of the liver. With artificial intelligence-based methodology, qFibrosis, we may provide a more reliable way to assess the FZHY as a therapy in chronic liver diseases because of its dual anti-inflammatory and antifibrotic properties.

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Tanabe, Kiwamu, Tatsuya Usui, and Kazuaki Sasaki. "Search for novel antifibrotic agents using nonalcoholic steatohepatitis (NASH) organoid model." Proceedings for Annual Meeting of The Japanese Pharmacological Society 95 (2022): 1—LBS—04. http://dx.doi.org/10.1254/jpssuppl.95.0_1-lbs-04.

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Rupcic Rubin, Vinka, Kristina Bojanic, Martina Smolic, Jurica Rubin, Ashraf Tabll, and Robert Smolic. "An Update on Efficacy and Safety of Emerging Hepatic Antifibrotic Agents." Journal of Clinical and Translational Hepatology 000, no. 000 (January 4, 2021): 1–11. http://dx.doi.org/10.14218/jcth.2020.00040.

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Ma, Zhen, Youlu Pan, Wenhai Huang, Yewei Yang, Zunyuan Wang, Qin Li, Yin Zhao, Xinyue Zhang, and Zhengrong Shen. "Synthesis and biological evaluation of the pirfenidone derivatives as antifibrotic agents." Bioorganic & Medicinal Chemistry Letters 24, no. 1 (January 2014): 220–23. http://dx.doi.org/10.1016/j.bmcl.2013.11.038.

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Tang, X., S. Teng, M. Petri, C. Krettek, C. Liu, and M. Jagodzinski. "The effect of anti-inflammatory and antifibrotic agents on fibroblasts obtained from arthrofibrotic tissue." Bone & Joint Research 7, no. 3 (March 2018): 213–22. http://dx.doi.org/10.1302/2046-3758.73.bjr-2017-0219.r2.

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Objectives The aims of this study were to determine whether the administration of anti-inflammatory and antifibrotic agents affect the proliferation, viability, and expression of markers involved in the fibrotic development of the fibroblasts obtained from arthrofibrotic tissue in vitro, and to evaluate the effect of the agents on arthrofibrosis prevention in vivo. Methods Dexamethasone, diclofenac, and decorin, in different concentrations, were employed to treat fibroblasts from arthrofibrotic tissue (AFib). Cell proliferation was measured by DNA quantitation, and viability was analyzed by Live/Dead staining. The levels of procollagen type I N-terminal propeptide (PINP) and procollagen type III N-terminal propeptide (PIIINP) were evaluated with enzyme-linked immunosorbent assay (ELISA) kits. In addition, the expressions of fibrotic markers were detected by real-time polymerase chain reaction (PCR). Fibroblasts isolated from healthy tissue (Fib) served as control. Further, a rabbit model of joint contracture was used to evaluate the antifibrotic effect of the three different agents. Results Dexamethasone maintained the viability and promoted the proliferation of AFib. Diclofenac decreased the viability and inhibited the cell proliferation during the first week of cultivation. However, decorin inhibited AFib proliferation and downregulated the expressions of fibrotic markers. Additionally, decorin could improve the flexion contracture angle and inhibit the deposition of interstitial matrix components in the rabbit joint model. Conclusion Decorin decreased the expression of myofibroblast markers in AFib, inhibited the proliferation of AFib, and prevented the initial procedure of arthrofibrosis in vivo, suggesting that decorin could be a promising treatment to inhibit the development of arthrofibrosis. Cite this article: X. Tang, S. Teng, M. Petri, C. Krettek, C. Liu, M. Jagodzinski. The effect of anti-inflammatory and antifibrotic agents on fibroblasts obtained from arthrofibrotic tissue: An in vitro and in vivo study. Bone Joint Res 2018;7:213–222. DOI: 10.1302/2046-3758.73.BJR-2017-0219.R2.

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Liang, Minrui, Eric L. Matteson, Andy Abril, and Jörg H. W. Distler. "The role of antifibrotics in the treatment of rheumatoid arthritis–associated interstitial lung disease." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2210744. http://dx.doi.org/10.1177/1759720x221074457.

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The major pulmonary complication of rheumatoid arthritis (RA) is interstitial lung disease (ILD), which causes significant morbidity and mortality and influences the natural course of disease. Recent advances in the management of arthritis have improved patient outcomes. However, exceptionally high medical needs still remain for effective therapies for the patients with ILD in RA. Better understanding of the shared and distinct pathophysiology of fibrotic diseases led to the development of novel antifibrotic agents such as nintedanib and pirfenidone. The further stratification analysis of the phase III INBUILD trial demonstrated beneficial effects of nintedanib in RA-ILD with a progressive phenotype by reducing the rate of decline in forced vital capacity (FVC) over 52 weeks by 60%. Pirfenidone is another antifibrotic agent currently under phase II clinical study (TRAIL1) aiming to evaluate its effects for RA-ILD. This review provides an overview of state-of-the-art pathogenesis and the current therapeutic options for RA-ILD, with a focus on antifibrotic strategies.

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Corrie, Leander, MD Muzaffar-Ur-Rehman, Latha Kukatil, Devasari Manasa, and Adepu Shirisha. "Antifibrotic Drugs for COVID-19: From Orphan Drugs to Blockbusters?" Current Respiratory Medicine Reviews 17, no. 1 (May 5, 2021): 8–12. http://dx.doi.org/10.2174/1573398x17666210304100043.

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: Antifibrotic agents are known to treat idiopathic pulmonary fibrosis. The two antifibrotic agents approved and in usage are Pirfenidone and Nintedanib granted by the USFDA in 2014. They are both known to decrease inflammation in the lungs. The fact that COVID-19 has shown to cause inflammation and fibrosis in the lungs frames the theory of their usage in the treatment of the disease by reducing lung scaring and allowing faster discharge of patients with post-COVID complications. The need for them to change their status from orphans to blockbusters has not happened yet due to fewer data and less research available on them as well as various other economic and patient- related factors. Since COVID-19 is widespread and causes many complications of the lungs that are similar to what these two drugs treat. We believe that the status of these drugs could be changed due to an increase in demand for them.

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Koga, Yasuhiko, Yoshimasa Hachisu, Hiroaki Tsurumaki, Masakiyo Yatomi, Kyoichi Kaira, Shoichiro Ohta, Junya Ono, Kenji Izuhara, Kunio Dobashi, and Takeshi Hisada. "Pirfenidone Improves Familial Idiopathic Pulmonary Fibrosis without Affecting Serum Periostin Levels." Medicina 55, no. 5 (May 17, 2019): 161. http://dx.doi.org/10.3390/medicina55050161.

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Background: Antifibrotic agents have been approved for the treatment of idiopathic pulmonary fibrosis (IPF). However, the efficacy of these drugs in the treatment of familial IPF (FIPF) has not been previously reported. Case presentation: We report the case of a 77-year-old man with FIPF, successfully treated with pirfenidone. His uncle died due to IPF, and his niece was diagnosed with the disease. He had worsening dyspnea two months prior to admission to our hospital. Upon admission, he had desaturation when exercising and broad interstitial pneumonia. Administration of pirfenidone improved his dyspnea, desaturation, and the reticular shadow on his chest radiograph. Increased fibrotic marker levels KL-6 and SP-D were also normalized in six months; treatment had no effect on his serum periostin level. Pirfenidone has been effective for over two years. Conclusion: Antifibrotic agents such as pirfenidone may be useful for the management of FIPF, as well as cases of sporadic IPF.

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Górska, Katarzyna, Marta Maskey-Warzęchowska, Małgorzata Barnaś, Adam Białas, Adam Barczyk, Hanna Jagielska-Len, Ewa Jassem, et al. "Therapeutic decisions in a cohort of patients with idiopathic pulmonary fibrosis: a multicenter, prospective survey from Poland." Therapeutic Advances in Chronic Disease 13 (January 2022): 204062232211179. http://dx.doi.org/10.1177/20406223221117982.

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Background: Pirfenidone and nintedanib are considered as the standard of care in idiopathic pulmonary fibrosis (IPF), but there is no consensus as to which of these two agents should be regarded as first-line treatment. Objective: To provide real-world data on therapeutic decisions of pulmonary specialists, particularly the choice of the antifibrotic drug in patients with IPF. Methods: This was a multicenter, prospective survey collecting clinical data of patients with IPF considered as candidates for antifibrotic treatment between September 2019 and December 2020. Clinical characteristics and information on the therapeutic approach were retrieved. Statistical evaluation included multiple logistic regression analysis with stepwise model selection. Results: Data on 188 patients [74.5% male, median age 73 (interquartile range, 68–78) years] considered for antifibrotic therapy were collected. Treatment was initiated in 138 patients, while 50 patients did not receive an antifibrotic, mainly due to the lack of consent for treatment and IPF severity. Seventy-two patients received pirfenidone and 66 received nintedanib. Dosing protocol ( p < 0.01) and patient preference ( p = 0.049) were more frequently associated with the choice of nintedanib, while comorbidity profile ( p = 0.0003) and concomitant medication use ( p = 0.03) were more frequently associated with the choice of pirfenidone. Age ( p = 0.002), lung transfer factor for carbon monoxide (TLCO) ( p = 0.001), and gastrointestinal bleeding ( p = 0.03) were significantly associated with the qualification for the antifibrotic treatment. Conclusion: This real-world prospective study showed that dose protocol and patient preference were more frequently associated with the choice of nintedanib, while the comorbidity profile and concomitant medication use were more frequently associated with the choice of pirfenidone. Age, TLCO, and history of gastrointestinal bleeding were significant factors influencing the decision to initiate antifibrotic therapy.

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Roman, Jesse, and Hirofumi Chiba. "B Cells in Idiopathic Pulmonary Fibrosis: Targeting Immune Cells with Antifibrotic Agents." American Journal of Respiratory Cell and Molecular Biology 64, no. 6 (June 2021): 652–54. http://dx.doi.org/10.1165/rcmb.2021-0101ed.

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Budenz, Donald L., Mark Pyfer, Kuldev Singh, Jeffrey Gordon, Jody Piltz-Seymour, and Edwin U. Keates. "Comparison of Phacotrabeculectomy With 5-Fluorouracil, Mitomycin-C, and Without Antifibrotic Agents." Ophthalmic Surgery, Lasers and Imaging Retina 30, no. 5 (May 1999): 367–74. http://dx.doi.org/10.3928/1542-8877-19990501-08.

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Adtani, Pooja, Narasimhan Malathi, Kannan Ranganathan, Sivaswamy Lokeswari, and Alan Mathew Punnoose. "Antifibrotic effect of Ocimum basilicum L. and linalool on arecoline-induced fibrosis in human buccal fibroblasts." Translational Research in Oral Oncology 3 (January 1, 2018): 2057178X1876447. http://dx.doi.org/10.1177/2057178x18764471.

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Aim: To explore Ocimum basilicum L. (sweet basil) and linalool for their antifibrotic activity in an arecoline-induced in vitro fibrotic model. Methods: Leaf extract of O. basilicum L. (LEOB) and linalool were used as experimental agents to test their antifibrogenic activity in vitro. Half-maximal inhibitory concentration (IC50) for arecoline, ethanolic LEOB, and linalool was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To evaluate the antifibrotic effect of ethanolic LEOB and linalool on pretreatment, that is, both the testing agents were added to the human buccal fibroblasts (HBFs) prior to induction with arecoline, and reverse transcriptase polymerase chain reaction (RT-PCR) was carried out to study the response of transforming growth factor beta (TGFβ), collagen 1 subtype A2 (COL1A2), and collagen 3 subtype A1 (COL3A1). To appreciate the morphological alterations in HBFs on treatment with arecoline, ethanolic LEOB, and linalool, Masson’s trichrome staining was performed. Results: Arecoline enhanced fibrotic activity by upregulating TGFβ1, COL1A2, and COL3A1 levels, whereas ethanolic LEOB and linalool on pretreatment significantly downregulated the increased levels of TGFβ1, COL1A2, and COL3A1 in primary HBF cell cultures. Conclusion and implication to clinic: Both ethanolic LEOB and linalool exhibited significant antifibrotic activity in an in vitro model. Further studies in an in vitro model can help attain a foundation for an herbal formulation in gel form that can be prescribed to patients diagnosed with oral submucous fibrosis for topical application. It can also be used synergistically with Western medicine.

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Lv, Wenshan, Fan Fan, Yangang Wang, Ezekiel Gonzalez-Fernandez, Chen Wang, Lili Yang, George W. Booz, and Richard J. Roman. "Therapeutic potential of microRNAs for the treatment of renal fibrosis and CKD." Physiological Genomics 50, no. 1 (January 1, 2018): 20–34. http://dx.doi.org/10.1152/physiolgenomics.00039.2017.

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Chronic kidney disease (CKD), defined as reduced glomerular filtration rate, is increasingly becoming a major public health issue. At the histological level, renal fibrosis is the final common pathway leading to end-stage renal disease, irrespective of the initial injury. According to this view, antifibrotic agents should slow or halt the progression of CKD. However, due to multiple overlapping pathways stimulating fibrosis, it has been difficult to develop antifibrotic drugs that delay or reverse the progression of CKD. MicroRNAs (miRNAs) are small noncoding RNA molecules, 18–22 nucleotides in length, that control many developmental and cellular processes as posttranscriptional regulators of gene expression. Emerging evidence suggests that miRNAs targeted against genes involved in renal fibrosis might be potential candidates for the development of antifibrotic therapies for CKD. This review will discuss some of the miRNAs, such as Let-7, miR-21,-29, -192, -200,-324, -132, -212, -30, -126, -433, -214, and -199a, that are implicated in renal fibrosis and the potential to exploit these molecular targets for the treatment of CKD.

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Skurikhin, Evgenii, Vladimir Nebolsin, Darius Widera, Natalia Ermakova, Olga Pershina, Angelina Pakhomova, Vyacheslav Krupin, et al. "Antifibrotic and Regenerative Effects of Treamid in Pulmonary Fibrosis." International Journal of Molecular Sciences 21, no. 21 (November 8, 2020): 8380. http://dx.doi.org/10.3390/ijms21218380.

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Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disease characterized by interstitial fibrosis and progressive respiratory failure. Pirfenidone and nintedanib slow down but do not stop the progression of IPF. Thus, new compounds with high antifibrotic activity and simultaneously regenerative activity are an unmet clinical need. Recently, we showed that Treamid can help restoring the pancreas and testicular tissue in mice with metabolic disorders. We hypothesized that Treamid may be effective in antifibrotic therapy and regeneration of damaged lung tissue in pulmonary fibrosis. In this study, experiments were performed on male C57BL/6 mice with bleomycin-induced pulmonary fibrosis. We applied histological and immunohistochemical methods, ELISA, and assessed the expression of markers of endothelial and epithelial cells in primary cultures of CD31+ and CD326+ lung cells. Finally, we evaluated esterase activity and apoptosis of lung cells in vitro. Our data indicate that Treamid exhibits antifibrotic activity in mice with pulmonary fibrosis and has a positive effect on capillaries of the lungs. Treamid also increases the number of endothelial progenitor cells in the lungs of animals with pulmonary fibrosis. Lastly, Treamid increases esterase activity and decreases apoptosis of CD31+ lung cells in vitro. Based on these findings, we suggest that Treamid may represent a promising compound for the development of new antifibrotic agents, which are capable of stimulating regeneration of lung endothelium in IPF patients.

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Burgess, Heather A., Louis Eugene Daugherty, Thomas H. Thatcher, Heather F. Lakatos, Denise M. Ray, Michelle Redonnet, Richard P. Phipps, and Patricia J. Sime. "PPARγ agonists inhibit TGF-β induced pulmonary myofibroblast differentiation and collagen production: implications for therapy of lung fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 6 (June 2005): L1146—L1153. http://dx.doi.org/10.1152/ajplung.00383.2004.

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Pulmonary fibrosis is a progressive life-threatening disease for which no effective therapy exists. Myofibroblasts are one of the key effector cells in pulmonary fibrosis and are the primary source of extracellular matrix production. Drugs that inhibit the differentiation of fibroblasts to myofibroblasts have potential as antifibrotic therapies. Peroxisome proliferator-activated receptor (PPAR)-γ is a transcription factor that upon ligation with PPARγ agonists activates target genes containing PPAR response elements. PPARγ agonists have anti-inflammatory activities and may have potential as antifibrotic agents. In this study, we examined the abilities of PPARγ agonists to block two of the most important profibrotic activities of TGF-β on pulmonary fibroblasts: myofibroblast differentiation and production of excess collagen. Both natural (15d-PGJ2) and synthetic (ciglitazone and rosiglitazone) PPARγ agonists inhibited TGF-β-driven myofibroblast differentiation, as determined by α-smooth muscle actin-specific immunocytochemistry and Western blot analysis. PPARγ agonists also potently attenuated TGF-β-driven type I collagen protein production. A dominant-negative PPARγ partially reversed the inhibition of myofibroblast differentiation by 15d-PGJ2 and rosiglitazone, but the irreversible PPARγ antagonist GW-9662 did not, suggesting that the antifibrotic effects of the PPARγ agonists are mediated through both PPARγ-dependent and independent mechanisms. Thus PPARγ agonists have novel and potent antifibrotic effects in human lung fibroblasts and may have potential for therapy of fibrotic diseases in the lung and other tissues.

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Kumai, Yoshihiko. "Pathophysiology of Fibrosis in the Vocal Fold: Current Research, Future Treatment Strategies, and Obstacles to Restoring Vocal Fold Pliability." International Journal of Molecular Sciences 20, no. 10 (May 24, 2019): 2551. http://dx.doi.org/10.3390/ijms20102551.

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Communication by voice depends on symmetrical vibrations within the vocal folds (VFs) and is indispensable for various occupations. VF scarring is one of the main reasons for permanent dysphonia and results from injury to the unique layered structure of the VFs. The increased collagen and decreased hyaluronic acid within VF scars lead to a loss of pliability of the VFs and significantly decreases their capacity to vibrate. As there is currently no definitive treatment for VF scarring, regenerative medicine and tissue engineering have become increasingly important research areas within otolaryngology. Several recent reviews have described the problem of VF scarring and various possible solutions, including tissue engineered cells and tissues, biomaterial implants, stem cells, growth factors, anti-inflammatory cytokines antifibrotic agents. Despite considerable research progress, these technical advances have not been established as routine clinical procedures. This review focuses on emerging techniques for restoring VF pliability using various approaches. We discuss our studies on interactions among adipose-derived stem/stromal cells, antifibrotic agents, and VF fibroblasts using an in vitro model. We also identify some obstacles to advances in research.

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Collins, Bridget F., and Ganesh Raghu. "Antifibrotic therapy for fibrotic lung disease beyond idiopathic pulmonary fibrosis." European Respiratory Review 28, no. 153 (September 30, 2019): 190022. http://dx.doi.org/10.1183/16000617.0022-2019.

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Two antifibrotic medications (nintedanib and pirfenidone) were recommended (conditionally) for the treatment of patients with idiopathic pulmonary fibrosis (IPF) in the 2015 IPF evidence-based guidelines. These medications have been shown to reduce the rate of decline in forced vital capacity among patients with IPF over time and are the only two disease-modulating pharmacological agents approved by regulatory agencies and available for clinical use worldwide. With the evolved standard of care for interstitial lung disease evaluation including routine use of high-resolution computed tomography, fibrotic lung diseases other than IPF are increasingly recognised. In addition, it is becoming evident that genetic and pathophysiological mechanisms as well as disease behaviour in patients manifesting other “non-IPF progressive fibrotic interstitial lung diseases” (non-IPF-PF) may be similar to those in patients with IPF. Thus, it is biologically plausible that pharmacological agents with antifibrotic properties may be efficacious in non-IPF-PF. Indeed, studies are underway or planned to assess the safety and efficacy of nintedanib or pirfenidone among patients with several non-IPF fibrotic lung diseases. In this review, we briefly summarise the use of pirfenidone and nintedanib in IPF as well as the rationale and potential for use of these medications in non-IPF-PF that are being investigated in ongoing and upcoming clinical trials.

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Morrow, Lee E., Daniel Hilleman, and Mark A. Malesker. "Management of patients with fibrosing interstitial lung diseases." American Journal of Health-System Pharmacy 79, no. 3 (October 5, 2021): 129–39. http://dx.doi.org/10.1093/ajhp/zxab375.

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Abstract Purpose This article summarizes the appropriate use and pharmacology of treatments for fibrosing interstitial lung diseases, with a specific focus on the antifibrotic agents nintedanib and pirfenidone. Summary The interstitial lung diseases are a heterogenous group of parenchymal lung disorders with a common feature—infiltration of the interstitial space with derangement of the normal capillary-alveolar anatomy. Diseases characterized by fibrosis of the interstitial space are referred to as the fibrosing interstitial lung diseases and often show progression over time: idiopathic pulmonary fibrosis is the most common fibrotic interstitial lung disease. Historically, therapies for fibrosing lung diseases have been limited in number, questionable in efficacy, and associated with potential harms. Food and Drug Administration (FDA) approval of the antifibrotic agents nintedanib and pirfenidone for idiopathic pulmonary fibrosis in 2014 heralded an era of reorganization of therapy for the fibrotic interstitial lung diseases. Subsequent investigations have led to FDA approval of nintedanib for systemic sclerosis–associated interstitial lung disease and interstitial lung diseases with a progressive phenotype. Although supportive care and pulmonary rehabilitation should be provided to all patients, the role(s) of immunomodulators and/or immune suppressing agents vary by the underlying disease state. Several agents previously used to treat fibrotic lung diseases (N-acetylcysteine, anticoagulation, and pulmonary vasodilators) lack efficacy or cause harm. Conclusion With the introduction of effective pharmacotherapy for fibrosing interstitial lung disease, pharmacists have an increasingly important role in the interdisciplinary team managing these patients.

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Zakaria, Sherin, and Alaa E. El-Sisi. "Daclatasvir and Sofosbuvir Mitigate Hepatic Fibrosis Through Downregulation of TNF-α / NF-κB Signaling Pathway." Current Molecular Pharmacology 13, no. 4 (November 2, 2020): 318–27. http://dx.doi.org/10.2174/1874467213666200116114919.

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Background: Hepatic fibrosis is the major issue in chronic liver diseases such as chronic hepatitis C virus (HCV). The newly approved direct acting antiviral (DAA) agents such as Sofosbuvir (SOF) and daclatasvir (DAC) have been found to be associated with decreased fibrotic markers in HCV patients. Aim: This study tried to explore whether the reported antifibrotic effect of these drugs is antiviral dependent or drug induced. Method: Hepatic fibrosis was induced by (0.5ml/kg) CCl4 IP twice a week for six weeks. SOF (20 mg/kg/d) and DAC (30 mg/kg/d) were added in the last four weeks of treatments. Liver functions, fibrotic markers such as Hyaluronic acid and metalloproteinase-9 were detected using immunoassay. The expression of TNF-α/NF-κB signaling pathway as well as Bcl-2 were done using immunoassay. Results: SOF and DAC exerted a potent antifibrotic effect evidenced by their activity against hyaluronic acid HA and metalloproteinase MMP-9 significantly (P≤0.001). This effect was further proved histopathologically where liver tissues from rats treated by drugs showed marked inhibition of collagen precipitation as well as inhibition of HSCs activation. This antifibrotic action was associated with decreased expression of TNF-α /NF-κB signaling pathway and induction of Bcl-2. Conclusion: SOF/ DAC antifibrotic effect is independent of its antiviral activity. The molecular events associated with this effect were the downregulation of TNF-α / NF-κB signaling pathway and induction of Bcl-2.

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Yang, Cheng-Chun, Chin-Yu Chen, Yu-Ting Kuo, Ching-Chung Ko, Wen-Jui Wu, Chia-Hao Liang, Chun-Ho Yun, and Wei-Ming Huang. "Radiomics for the Prediction of Response to Antifibrotic Treatment in Patients with Idiopathic Pulmonary Fibrosis: A Pilot Study." Diagnostics 12, no. 4 (April 15, 2022): 1002. http://dx.doi.org/10.3390/diagnostics12041002.

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Antifibrotic therapy has changed the treatment paradigm for idiopathic pulmonary fibrosis (IPF); however, a subset of patients still experienced rapid disease progression despite treatment. This study aimed to determine whether CT-based radiomic features can predict therapeutic response to antifibrotic agents. In this retrospective study, 35 patients with IPF on antifibrotic treatment enrolled from two centers were divided into training (n = 26) and external validation (n = 9) sets. Clinical and pulmonary function data were collected. The patients were categorized into stable disease (SD) and progressive disease (PD) groups based on functional or radiologic criteria. From pretreatment non-enhanced high-resolution CT (HRCT) images, twenty-six radiomic features were extracted through whole-lung texture analysis, and six parenchymal patterns were quantified using dedicated imaging platforms. The predictive factors for PD were determined via univariate and multivariate logistic regression analyses. In the training set (SD/PD: 12/14), univariate analysis identified eight radiomic features and ground-glass opacity percentage (GGO%) as potential predicators of PD. However, multivariate analysis found that the single independent predictor was the sum entropy (accuracy, 80.77%; AUC, 0.75). The combined sum entropy-GGO% model improved the predictive performance in the training set (accuracy, 88.46%; AUC, 0.77). The overall accuracy of the combined model in the validation set (SD/PD: 7/2) was 66.67%. Our preliminary results demonstrated that radiomic features based on pretreatment HRCT could predict the response of patients with IPF to antifibrotic treatment.

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Duval, Florent, Jorge E. Moreno-Cuevas, Maria Teresa González-Garza, Carlos Rodríguez-Montalvo, and Delia Elva Cruz-Vega. "Liver Fibrosis and Protection Mechanisms Action of Medicinal Plants Targeting Apoptosis of Hepatocytes and Hepatic Stellate Cells." Advances in Pharmacological Sciences 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/373295.

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Following chronic liver injury, hepatocytes undergo apoptosis leading to activation of hepatic stellate cells (HSC). Consequently, activated HSC proliferate and produce excessive extracellular matrix, responsible for the scar formation. The pandemic trend of obesity, combined with the high incidence of alcohol intake and viral hepatitis infections, highlights the urgent need to find accessible antifibrotic therapies. Treatment strategies should take into account the versatility of its pathogenesis and act on all the cell lines involved to reduce liver fibrosis. Medicinal plants are achieving popularity as antifibrotic agents, supported by their safety, cost-effectiveness, and versatility. This review will describe the role of hepatocytes and HSC in the pathogenesis of liver fibrosis and detail the mechanisms of modulation of apoptosis of both cell lines by twelve known hepatoprotective plants in order to reduce liver fibrosis.

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Duval, Florent, Jorge E. Moreno-Cuevas, María Teresa González-Garza, Carmen Maldonado-Bernal, and Delia Elva Cruz-Vega. "Liver Fibrosis and Mechanisms of the Protective Action of Medicinal Plants Targeting Inflammation and the Immune Response." International Journal of Inflammation 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/943497.

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Inflammation is a central feature of liver fibrosis as suggested by its role in the activation of hepatic stellate cells leading to extracellular matrix deposition. During liver injury, inflammatory cells are recruited in the injurious site through chemokines attraction. Thus, inflammation could be a target to reduce liver fibrosis. The pandemic trend of obesity, combined with the high incidence of alcohol intake and viral hepatitis infections, highlights the urgent need to find accessible antifibrotic therapies. Medicinal plants are achieving popularity as antifibrotic agents, supported by their safety, cost-effectiveness, and versatility. The aim of this review is to describe the role of inflammation and the immune response in the pathogenesis of liver fibrosis and detail the mechanisms of inhibition of both events by medicinal plants in order to reduce liver fibrosis.

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Knobloch, K., A. Gohritz, M. Spies, and P. M. Vogt. "ACE inhibitors as antifibrotic agents in atrial fibrillation: potential relevance in cardiac surgery." Interactive CardioVascular and Thoracic Surgery 7, no. 3 (March 26, 2008): 475–76. http://dx.doi.org/10.1510/icvts.2007.174698a.

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Raja, S. G. "ACE inhibitors as antifibrotic agents in atrial fibrillation: potential relevance in cardiac surgery." Interactive CardioVascular and Thoracic Surgery 7, no. 3 (March 26, 2008): 476. http://dx.doi.org/10.1510/icvts.2007.174698a1.

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Cassone, Giulia, Andreina Manfredi, Caterina Vacchi, Fabrizio Luppi, Francesca Coppi, Carlo Salvarani, and Marco Sebastiani. "Treatment of Rheumatoid Arthritis-Associated Interstitial Lung Disease: Lights and Shadows." Journal of Clinical Medicine 9, no. 4 (April 10, 2020): 1082. http://dx.doi.org/10.3390/jcm9041082.

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Rheumatoid arthritis (RA) is a chronic and systemic inflammatory disease affecting 0.5–1% of the population worldwide. Interstitial lung disease (ILD) is a serious pulmonary complication of RA and it is responsible for 10–20% of mortality, with a mean survival of 5–8 years. However, nowadays there are no therapeutic recommendations for the treatment of RA-ILD. Therapeutic options for RA-ILD are complicated by the possible pulmonary toxicity of many disease modifying anti-rheumatic drugs (DMARDs) and by their unclear efficacy on pulmonary disease. Therefore, joint and lung involvement should be evaluated independently of each other for treatment purposes. On the other hand, some similarities between RA-ILD and idiopathic pulmonary fibrosis and the results of the recent INBIULD trial suggest a possible future role for antifibrotic agents. From this perspective, we review the current literature describing the pulmonary effects of drugs (immunosuppressants, conventional, biological and target synthetic DMARDs and antifibrotic agents) in patients with RA and ILD. In addition, we suggest a framework for the management of RA-ILD patients and outline a research agenda to fill the gaps in knowledge about this challenging patient cohort.

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Hewitson, Tim D. "Renal tubulointerstitial fibrosis: common but never simple." American Journal of Physiology-Renal Physiology 296, no. 6 (June 2009): F1239—F1244. http://dx.doi.org/10.1152/ajprenal.90521.2008.

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Regardless of etiology, all patients with chronic renal disease show a progressive decline in renal function with time. Fibrosis, so-called scarring, is a key cause of this pathophysiology. Fibrosis involves an excess accumulation of extracellular matrix (primarily composed of collagen) and usually results in loss of function when normal tissue is replaced with scar tissue. While recent major advances have led to a much better understanding of this process, many problems remain. We for instance know little about why some wounds heal and others scar and little about how many putative antifibrotic agents work. This review discusses recent advances in our understanding of the mechanisms of tubulointerstitial fibrosis, focusing on the regulation and role of the myofibroblast in this process, the role of recently recognized endogenous antifibrotic factors, controversy surrounding the effects of metalloproteinases, and the opportunities presented by new treatment strategies that abrogate and may even reverse fibrosis.

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Turan, Onur, and Bünyamin Sertoğullarından. "Efficacy and tolerability of antifibrotic agents in idiopathic pulmonary fibrosis: An experience from Turkey." Eurasian Journal of Pulmonology 23, no. 1 (2021): 59. http://dx.doi.org/10.4103/ejop.ejop_74_20.

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Schnabl, Bernd, David Scholten, and David A. Brenner. "What is the potential role of antifibrotic agents for the treatment of liver disease?" Nature Clinical Practice Gastroenterology & Hepatology 5, no. 9 (July 15, 2008): 496–97. http://dx.doi.org/10.1038/ncpgasthep1200.

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Liu, Xiaoqiu, Rennolds S. Ostrom, and Paul A. Insel. "cAMP-elevating agents and adenylyl cyclase overexpression promote an antifibrotic phenotype in pulmonary fibroblasts." American Journal of Physiology-Cell Physiology 286, no. 5 (May 2004): C1089—C1099. http://dx.doi.org/10.1152/ajpcell.00461.2003.

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Pulmonary fibroblasts are recruited to sites of lung injury, where they are activated to produce extracellular matrix proteins and to facilitate repair. However, these cells become dysregulated in pulmonary fibrosis, producing excess collagen at sites of injury and forming fibrotic loci that impair lung function. In this study, we used WI-38 human lung fibroblasts and evaluated the ability of G protein-coupled receptor agonists to increase cAMP production and regulate cell proliferation and collagen synthesis. WI-38 cells increase cAMP in response to the β-adrenergic agonist isoproterenol (Iso), prostaglandin E2 (PGE2), certain prostanoid receptor-selective agonists (beraprost, butaprost), an adenosine receptor agonist, and the direct adenylyl cyclase (AC) activator forskolin (Fsk). Responses to Iso, PGE2, and Fsk were studied in more detail. Each induced a dose-dependent inhibition of serum-stimulated cell proliferation (as measured by [3H]thymidine incorporation) and collagen synthesis (as measured by [3H]proline incorporation, collagenase-sensitive [3H]proline incorporation, or levels of procollagen type 1 C-peptide). Quantitative RT-PCR analyses indicated that elevation in cellular cAMP levels decreases expression of collagen types 1α(II) and 5α(I) and increases expression and activity of matrix metalloproteinase 2 (MMP-2). Overexpression of AC type 6 or inhibition of cyclic nucleotide phosphodiesterases also increased cellular cAMP levels and decreased cell proliferation and collagen synthesis. Thus multiple approaches that increase cAMP signaling reduce proliferation and differentiated function in human pulmonary fibroblasts. These results suggest that therapies that raise cAMP levels may prove useful in the treatment of pulmonary fibrosis.

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SOLOMON, ABRAHAM, URIEL TICHO, and JOSEPH FRUCHT-PERY. "Late-Onset, Bleb-Associated Endophthalmitis following Glaucoma Filtering Surgery with or without Antifibrotic Agents." Journal of Ocular Pharmacology and Therapeutics 15, no. 4 (August 1999): 283–93. http://dx.doi.org/10.1089/jop.1999.15.283.

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Lee, Y. S., K. Y. Kim, B. S. Yu, K. S. Kil, J. Y. Jeong, J. J. Cho, and J. H. Che. "Development of hepatic fibrosis (cirrhosis) model in rats and screening of the antifibrotic agents." Toxicology Letters 95 (July 1998): 165. http://dx.doi.org/10.1016/s0378-4274(98)80660-7.

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Law, Simon K. "A Modified Technique of Ahmed Glaucoma Valve Implantation with Adjunctive Use of Antifibrotic Agents." American Journal of Ophthalmology 146, no. 2 (August 2008): 156–58. http://dx.doi.org/10.1016/j.ajo.2008.05.003.

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Baxter, Ruth M., Thomas P. Crowell, Margaret E. McCrann, Erica M. Frew, and Humphrey Gardner. "Analysis of the tight skin (Tsk1/+) mouse as a model for testing antifibrotic agents." Laboratory Investigation 85, no. 10 (August 15, 2005): 1199–209. http://dx.doi.org/10.1038/labinvest.3700331.

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Taufiq, Ahmad, Rosy Eko Saputro, Hendra Susanto, Nurul Hidayat, Sunaryono Sunaryono, Tahta Amrillah, Husni Wahyu Wijaya, Nandang Mufti, and Firman Mangasa Simanjuntak. "Synthesis of Fe3O4/Ag nanohybrid ferrofluids and their applications as antimicrobial and antifibrotic agents." Heliyon 6, no. 12 (December 2020): e05813. http://dx.doi.org/10.1016/j.heliyon.2020.e05813.

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Journal articles on the topic 'Antifibrotic Agents'

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