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. |
| NCT00011076 ↗ | Pirfenidone to Treat Hypertrophic Cardiomyopathy | Completed | National Heart, Lung, and Blood Institute (NHLBI) | Phase 2 | 2001-02-01 | This study will examine the effectiveness of the drug pirfenidone (Deskar) in improving heart function in patients with hypertrophic cardiomyopathy (HCM). Stiffening of the heart muscle in patients with HCM impairs the heart's ability to relax and thus fill and empty properly. This can lead to heart failure, breathlessness and excessive fatigue. The heart's inability to relax may be due to scarring, or fibrosis, in the muscle wall. This study will test whether pirfenidone can reduce fibrosis, improve heart relaxation and reduce abnormal heart rhythms. Men and women 20 to 75 years old with HCM may be eligible for this study. Participants will undergo a physical examination, blood tests, and other tests and procedures, described below, to assess heart function. When the tests are completed, patients will be randomly assigned to one of two treatment groups. One group will take a pirfenidone capsule and the other will take a placebo (a look-alike pill with no active ingredient) twice a day with meals for 6 months. For the pirfenidone group, the dose of drug will be increased gradually from 400 to 800 milligrams. At the end of 6 months, all patients will repeat the physical examination and heart tests that were done before starting medication. These include: - Electrocardiogram (ECG) - electrodes are attached to the heart to record the heart's electrical activity, providing information on the heartbeat. - Echocardiogram - a probe held against the chest wall uses sound waves to produce images of the heart, providing information on the function of the heart chambers. - 24-hour Holter monitor - a 24-hour recording of the electrical activity of the heart monitors for abnormal heartbeats or conduction abnormalities. - Magnetic resonance imaging (MRI) - Radiowaves and a strong magnetic field are used to produce images of the heart, providing information on the thickness and movement of the heart muscle. - Radionuclide angiogram - a radioactive tracer is injected into a vein and a special camera is used to scan the heart, providing information on the beating motion of the heart. Scans are obtained at rest and after exercise. - Cardiac (heart) catheterization - a catheter (thin plastic tube) is inserted into a blood vessel in the groin and advanced to the heart to record pressures and take pictures inside the heart. - Electrophysiology study - a catheter is inserted into a blood vessel in the groin and advanced to the heart to record electrical activity, providing information on abnormal heart rhythms. This procedure is done at the time of the heart catheterization. - Cardiac biopsy - a catheter is inserted into a blood vessel in the groin and advanced to the heart to remove a small sample of heart muscle for microscopic examination. This procedure is done at the end of the heart catheterization. |
| NCT00020631 ↗ | Pirfenidone in Treating Patients With Fibrosis Caused by Radiation Therapy for Cancer | Completed | National Cancer Institute (NCI) | N/A | 2001-10-01 | RATIONALE: Pirfenidone may prevent or lessen fibrosis caused by radiation therapy. PURPOSE: Pilot trial to study the effectiveness of pirfenidone in preventing or lessening fibrosis in patients who have undergone radiation therapy for cancer. |
| NCT00053937 ↗ | Pirfenidone in Treating Young Patients With Neurofibromatosis Type 1 and Plexiform Neurofibromas | Completed | National Cancer Institute (NCI) | Phase 1 | 2002-12-01 | RATIONALE: Chemoprevention therapy is the use of certain drugs to try to prevent the development or recurrence of cancer. Pirfenidone may slow the growth or prevent further development of plexiform neurofibromas. PURPOSE: Phase I trial to study the effectiveness of pirfenidone in treating young patients who have neurofibromatosis type 1 and plexiform neurofibroma. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
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