CLINICAL TRIALS PROFILE FOR PIRFENIDONE
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505(b)(2) Clinical Trials for PIRFENIDONE
| Trial Type | Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|---|
| New Formulation | NCT02408744 ↗ | Utility of Prolonged-release Pirfenidone in the Progression of Chronic Kidney Disease | Completed | Cell Therapy And Technology, S.a. De C.v. | Phase 1/Phase 2 | 2009-09-01 | The aim of this study was to evaluate the impact in safety and efficacy of a new formulation of prolonged-released Pirfenidone in the progression of renal damage in patients with Chronic kidney Disease (CKD). |
| New Formulation | NCT02408744 ↗ | Utility of Prolonged-release Pirfenidone in the Progression of Chronic Kidney Disease | Completed | University of Guadalajara | Phase 1/Phase 2 | 2009-09-01 | The aim of this study was to evaluate the impact in safety and efficacy of a new formulation of prolonged-released Pirfenidone in the progression of renal damage in patients with Chronic kidney Disease (CKD). |
| >Trial Type | >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
All Clinical Trials for PIRFENIDONE
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00001596 ↗ | Oral Pirfenidone for the Pulmonary Fibrosis of Hermansky-Pudlak Syndrome | Completed | National Human Genome Research Institute (NHGRI) | Phase 2 | 2005-09-01 | Hermansky-Pudlak Syndrome (HPS) is an inherited disease that results in decreased pigmentation (oculocutaneous albinism), bleeding problems due to a platelet abnormality (platelet storage pool defect), and storage of an abnormal fat-protein compound (lysosomal accumulation of ceroid lipofuscin). The disease can cause poor functioning of the lungs, intestine, kidneys, or heart. The most serious complication of the disease is pulmonary fibrosis and typically causes death in patients 40 - 50 years old. The disorder is common in Puerto Rico, where many of the clinical research studies on the disease have been conducted. Neither the full extent of the disease nor the basic cause of the disease is known. There is no known treatment for HPS. The drug pirfenidone blocks the biochemical process of inflammation and has been reported to slow or reverse pulmonary fibrosis in animal systems. In this study researchers will select up to 40 HPS patients diagnosed with pulmonary fibrosis. The patients will be randomly divided into 2 groups. The patients will not know if they are taking pirfenidone or a placebo "sugar pill". 1. Group one will be patients who will receive pirfenidone. 2. Group two will be patients who will receive a placebo "sugar pill" The major outcome measurement of the therapy will be a change in the lung function (forced vital capacity). The study will be stopped if one therapy proves to be more effective than the other. |
| NCT00001596 ↗ | Oral Pirfenidone for the Pulmonary Fibrosis of Hermansky-Pudlak Syndrome | Completed | William Gahl, M.D. | Phase 2 | 2005-09-01 | Hermansky-Pudlak Syndrome (HPS) is an inherited disease that results in decreased pigmentation (oculocutaneous albinism), bleeding problems due to a platelet abnormality (platelet storage pool defect), and storage of an abnormal fat-protein compound (lysosomal accumulation of ceroid lipofuscin). The disease can cause poor functioning of the lungs, intestine, kidneys, or heart. The most serious complication of the disease is pulmonary fibrosis and typically causes death in patients 40 - 50 years old. The disorder is common in Puerto Rico, where many of the clinical research studies on the disease have been conducted. Neither the full extent of the disease nor the basic cause of the disease is known. There is no known treatment for HPS. The drug pirfenidone blocks the biochemical process of inflammation and has been reported to slow or reverse pulmonary fibrosis in animal systems. In this study researchers will select up to 40 HPS patients diagnosed with pulmonary fibrosis. The patients will be randomly divided into 2 groups. The patients will not know if they are taking pirfenidone or a placebo "sugar pill". 1. Group one will be patients who will receive pirfenidone. 2. Group two will be patients who will receive a placebo "sugar pill" The major outcome measurement of the therapy will be a change in the lung function (forced vital capacity). The study will be stopped if one therapy proves to be more effective than the other. |
| NCT00001959 ↗ | Pirfenidone to Treat Kidney Disease (Focal Segmental Glomerulosclerosis) | Completed | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) | Phase 2 | 1999-12-01 | This study will examine the effectiveness of the drug pirfenidone in treating focal segmental glomerulosclerosis (FSGS). Patients with this disease have kidney fibrosis (scarring) and proteinuria (excessive excretion of protein in the urine). About half of patients with FSGS eventually require kidney dialysis or transplant. Steroids, which are currently used to treat the disease, are effective in only a minority of patients. Other drugs, such as cyclosporin and cyclophosphamide, improve proteinuria in a very small percentage of patients and have serious side effects. Patients with FSGS who wish to participate in this study will undergo pre-study evaluation with blood and urine tests. Patients must be on a stable dose of an ACE inhibitor (a drug that lowers blood pressure and reduces proteinuria) for at list 6 months before starting pirfenidone therapy. (Patients who are not already taking an ACE inhibitor will be started on the drug; those who cannot tolerate ACE inhibitors will be given a different drug.) Patients with elevated cholesterol will take a cholesterol-lowering drug. A diet containing approximately 1 gram of protein per kilogram of body weight per day will be recommended. Patients will take pirfenidone by mouth 3 times a day for 12 months. Blood and urine will be tested once a month, either at NIH or by the patient's local kidney specialist. They will collect two 24-hour urine samples at the beginning of the treatment period, at 2-month intervals throughout the study, and at a 6-month follow-up. Patients will also be asked to give three to five tubes of blood and urine samples for analysis during the study. In animal studies, pirfenidone improved kidney function and proteinuria and reduced kidney scarring in rats with a disease similar to FSGS. In human studies, pirfenidone improved breathing and survival in patients with lung fibrosis. |
| NCT00007475 ↗ | Permeability Factor in Focal Segmental Glomerulosclerosis | Completed | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) | Phase 1/Phase 2 | 2000-12-01 | Focal segmental glomerulosclerosis (FSGS) is a renal syndrome characterized by proteinuria (usually nephrotic range), limited response to conventional therapy, and a poor renal prognosis, with progression to end stage renal failure in at least 50% of patients. As a syndrome, FSGS likely has many specific etiologies, only a few of which are well-defined. Recently, it has been suggested that some idiopathic FSGS patients have elevated circulating levels of a protein that induces glomerular permeability in vitro and in vivo. While there has been no consistent term for this factor, it will be termed here FSGS permeability factor (FPF). The purposes of the present study are five fold: 1. To identify a population of FSGS patients with elevated FPF levels 2. To examine RNA expression profiles of peripheral blood mononuclear cells (PBMC) in FSGS patients with elevated FPF levels 3. To define the kinetics of FPF disappearance and reappearance in FSGS patients receiving immunomodulatory therapy and in the case of patients with recurrent FSGS following renal transplant, those receiving plasma exchange 4. To identify immunosuppressive agents which are successful in inducing sustained reduction in FPF levels 5. To determine in patients with FSGS who are awaiting renal transplant, whether sustained reduction in FPF levels is associated with reduced risk of recurrent FSGS. Patient participation is divided into an evaluation phase, in which FPF levels, RNA expression profiles, and patient eligibility for participation in treatment protocols are determined, and a treatment phase in which specific immunomodulatory therapy is introduced in an open label fashion. We propose to define carefully the relationship between elevated FPF and remission of proteinuria in patients with FSGS in native kidneys, following treatment with standard therapies (daily prednisone, cyclophosphamide) and experimental therapies (pulse dexamethasone, pirfenidone). In patients with recurrent FSGS in renal allografts, we will determine the kinetics of FPF following plasma exchange and following plasma exchange plus cyclophosphamide. In patients with elevated FPF levels who are awaiting renal transplantation, we will determine the kinetics of FPF following plasma exchange and following plasma exchange plus cyclophosphamide, and examine the rate of recurrent FSGS in these patients. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
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