Sunitinib Malate to Treat Advanced Eye Disease in Patients With Von Hippel-Lindau Syndrome
NCT ID: NCT00673816
Last Updated: 2024-01-05
Study Results
Results available
Outcome measurements, participant flow, baseline characteristics, and adverse events have been published for this study.
View full resultsBasic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
Recruitment Status
TERMINATED
Clinical Phase
PHASE1/PHASE2
Total Enrollment
2 participants
Study Classification
INTERVENTIONAL
Study Start Date
2008-05-31
Study Completion Date
2011-02-28
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
This open-label study will pilot the use of systemic sunitinib malate, a dual inhibitor of vascular endothelial growth factor (VEGF) and platelet derived growth factor (PDGF), in five participants with Von Hippel-Lindau (VHL) to investigate its potential efficacy as a treatment for retinal angiomas. Participants will have visual dysfunction with either visual acuity loss or visual field loss from retinal angiomas secondary to genetically confirmed VHL. This open-label study will pilot the use of systemic sunitinib malate in five participants to investigate its potential efficacy as a treatment for retinal angiomas associated with VHL. Participants will receive nine months of sunitinib malate therapy (six cycles total - one cycle consists of 50 mg oral dose once daily for four weeks followed by a two week rest period). The primary outcome will be a change in the best-corrected visual acuity of more than or equal to 15 letters from baseline to the Week 36 visit. The secondary ocular outcomes will focus on retinal thickness and leakage of the retinal angioma at the Week 36 visit. Optical coherence tomography will document changes in retinal thickening and fluorescein angiography will be used to determine leakage of the retinal angioma.
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
EYE001 to Treat Retinal Tumors in Patients With Von Hippel-Lindau Syndrome
NCT00056199
Hippel-Lindau Disease
COMPLETED
PHASE1
A Depot Formulation of Sunitinib Malate (GB-102) in Subjects With Neovascular (Wet) Age-related Macular Degeneration
NCT03249740
Neovascular Age-Related Macular Degeneration
COMPLETED
PHASE1
A Depot Formulation of Sunitinib Malate (GB-102) in Subjects With Diabetic Macular Edema and Retinal Vein Occlusion
NCT04085341
Diabetic Macular Edema
Retina Vein Occlusion
COMPLETED
PHASE2
Anti-VEGF Therapy for Subfoveal Hemorrhage in Patients With Neovascular Age-Related Macular Degeneration
NCT03699618
Submacular Hemorrhage
Wet Macular Degeneration
Neovascular Age-related Macular Degeneration
TERMINATED
Intravitreal Aflibercept Injections In The Treatment Of Pattern Dystrophy
NCT01965041
Pattern Dystrophy of Macula
WITHDRAWN
NA
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Von Hippel-Lindau Syndrome
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
Allocation Method
NA
Intervention Model
SINGLE_GROUP
Primary Study Purpose
TREATMENT
Blinding Strategy
NONE
Study Groups
Review each arm or cohort in the study, along with the interventions and objectives associated with them.
Sunitinib Malate
Participants were expected to receive 9 months of sunitinib malate therapy administered in 6 cycles. Each cycle consisted of a daily oral dose of 50 mg sunitinib malate for 4 weeks followed by a 2-week rest period).
Group Type
EXPERIMENTAL
Sunitinib Malate
Intervention Type
DRUG
Participants were expected to receive 9 months of sunitinib malate therapy administered in 6 cycles. Each cycle consisted of a daily oral dose of 50 mg sunitinib malate for 4 weeks followed by a 2-week rest period).
Interventions
Learn about the drugs, procedures, or behavioral strategies being tested and how they are applied within this trial.
Sunitinib Malate
Participants were expected to receive 9 months of sunitinib malate therapy administered in 6 cycles. Each cycle consisted of a daily oral dose of 50 mg sunitinib malate for 4 weeks followed by a 2-week rest period).
Intervention Type
DRUG
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
1. Participant must understand and sign the informed consent.
2. Participant must be at least 18 years of age.
3. Participant must have genetically confirmed VHL disease.
4. Participant must have an optic nerve angioma secondary to VHL in one or both eyes.
5. Participant must have an optic nerve tumor that has caused any visual field depression on microperimetry-1 that correlates with the retinal angioma OR the participant clinically may have hard exudates correlating with the retinal angioma OR has best-corrected visual acuity of 20/40 or worse in the study eye.
6. Participant must have clear ocular media and adequate pupillary dilation to permit good quality stereoscopic fundus photography.
7. All women of childbearing potential must have a negative urine pregnancy test at baseline, and have regular negative pregnancy testing while taking sunitinib malate. (Sunitinib malate has the potential for teratogenic or abortifacient effects, and no data regarding its safety in pregnant women are available).
8. All women of childbearing potential who are sexually active and all men who are sexually active are required to use two forms of birth control during the course of the study.
9. Participants must have normal organ and marrow function as defined below: WBC count ≥ 3,000/µL, absolute neutrophil count ≥ 1,500/µL, platelet count ≥ 100,000/µL, HGB\> 10g/dl, serum creatinine ≤ 2.0 or measured 24 hr. creatinine clearance \> 50 ml/min, AST and ALT \< 2.5 x ULN, total bilirubin ≤ ULN (\< 3 x NL in participants with Gilbert's disease).
10. Participant must have a negative HbsAg and nonreactive HCV.
11. Participant must have a negative HIV-1, as potential pharmacokinetic interactions of drugs used to treat HIV, such as anti-retroviral drugs, with sunitinib malate are unknown.
12. Participant must be at least four weeks from completion of any investigational therapy for VHL.
13. Participant must have an ECOG performance score of 0-2. (See Appendix 3 - ECOG Performance Criteria).
14. Participant has recovered from the acute toxicities of prior treatment for VHL.
2. Participant must be at least 18 years of age.
3. Participant must have genetically confirmed VHL disease.
4. Participant must have an optic nerve angioma secondary to VHL in one or both eyes.
5. Participant must have an optic nerve tumor that has caused any visual field depression on microperimetry-1 that correlates with the retinal angioma OR the participant clinically may have hard exudates correlating with the retinal angioma OR has best-corrected visual acuity of 20/40 or worse in the study eye.
6. Participant must have clear ocular media and adequate pupillary dilation to permit good quality stereoscopic fundus photography.
7. All women of childbearing potential must have a negative urine pregnancy test at baseline, and have regular negative pregnancy testing while taking sunitinib malate. (Sunitinib malate has the potential for teratogenic or abortifacient effects, and no data regarding its safety in pregnant women are available).
8. All women of childbearing potential who are sexually active and all men who are sexually active are required to use two forms of birth control during the course of the study.
9. Participants must have normal organ and marrow function as defined below: WBC count ≥ 3,000/µL, absolute neutrophil count ≥ 1,500/µL, platelet count ≥ 100,000/µL, HGB\> 10g/dl, serum creatinine ≤ 2.0 or measured 24 hr. creatinine clearance \> 50 ml/min, AST and ALT \< 2.5 x ULN, total bilirubin ≤ ULN (\< 3 x NL in participants with Gilbert's disease).
10. Participant must have a negative HbsAg and nonreactive HCV.
11. Participant must have a negative HIV-1, as potential pharmacokinetic interactions of drugs used to treat HIV, such as anti-retroviral drugs, with sunitinib malate are unknown.
12. Participant must be at least four weeks from completion of any investigational therapy for VHL.
13. Participant must have an ECOG performance score of 0-2. (See Appendix 3 - ECOG Performance Criteria).
14. Participant has recovered from the acute toxicities of prior treatment for VHL.
Exclusion Criteria
1. Participant has a history (within past five years) or evidence of severe cardiac disease including heart failure that meets New York Heart Association (NYHA) class III and IV definitions, uncontrolled dysrhythmias, dysrhythmias requiring anti-arhythmic drugs or has active ischemic heart disease including myocardial infarction and poorly controlled angina within 12 months of study entry.
2. Participant has a history of serious ventricular arrhythmia (ventricular tachycardia or ventricular fibrillation, ≥ three beats in a row) or left ventricular ejection fraction ≤ 40%.
3. Participant has a history of serious intercurrent medical illness.
4. Participant had transient ischemic attacks or cerebrovascular accident within 12 months of study entry.
5. Participant has hypertension that cannot be controlled with medications (persistent elevation of systolic BP \> 150 or diastolic BP \> 100 mmHg despite optimal medical therapy).
6. Participant is on therapeutic anticoagulation, including aspirin.
7. Participant who is breast-feeding, as there is an unknown but potential risk for adverse events in nursing infants secondary to treatment of the mother with sunitinib malate.
8. Participant has received any major surgical procedures within one month of study entry or has surgical scars that have not healed.
9. Participant has a known serious allergy to fluorescein dye.
10. Participant is currently taking drugs or ingesting food that affect sunitinib malate plasma concentrations: strong inhibitors of the CYP3A4 family (e.g., ketoconazole, itraconazole, clarithromycin, atazanavir, indinavir, nefazodone, nelfinavir, ritonavir, saquinavir, telithromycin, voriconazole, grapefruit juice) and/or inducers of the CYP3A4 family (e.g., dexamethasone, phenytoin, carbamazepine, rifampin, rifabutin, rifapentin, phenobarbital, St. John's Wort).
11. Participant has had a prior or concomitant non-VHL-associated malignancy with the exception of adequately treated basal or squamous cell carcinoma of the skin or any other malignancy from which the patient has remained disease free for more than five years.
12. Participant has had chemotherapy or radiotherapy within four weeks (six weeks for nitrosoureas or mitomycin C) prior to entering the study or those who have not recovered from adverse events (to Grade 1 or less toxicity according to CTCAE 3.0) due to agents administered more than four weeks earlier.
13. Participant is receiving other investigational agents.
14. Participants with known brain metastases (except when adequately controlled, i.e., have not grown in size, for ≥ 6 months before enrollment), not including hemangioblastoma, a known VHL complication of the brain.
15. Participant has a known bleeding disorder.
16. Participant is currently taking sunitinib malate or has taken sunitinib malate in the past.
2. Participant has a history of serious ventricular arrhythmia (ventricular tachycardia or ventricular fibrillation, ≥ three beats in a row) or left ventricular ejection fraction ≤ 40%.
3. Participant has a history of serious intercurrent medical illness.
4. Participant had transient ischemic attacks or cerebrovascular accident within 12 months of study entry.
5. Participant has hypertension that cannot be controlled with medications (persistent elevation of systolic BP \> 150 or diastolic BP \> 100 mmHg despite optimal medical therapy).
6. Participant is on therapeutic anticoagulation, including aspirin.
7. Participant who is breast-feeding, as there is an unknown but potential risk for adverse events in nursing infants secondary to treatment of the mother with sunitinib malate.
8. Participant has received any major surgical procedures within one month of study entry or has surgical scars that have not healed.
9. Participant has a known serious allergy to fluorescein dye.
10. Participant is currently taking drugs or ingesting food that affect sunitinib malate plasma concentrations: strong inhibitors of the CYP3A4 family (e.g., ketoconazole, itraconazole, clarithromycin, atazanavir, indinavir, nefazodone, nelfinavir, ritonavir, saquinavir, telithromycin, voriconazole, grapefruit juice) and/or inducers of the CYP3A4 family (e.g., dexamethasone, phenytoin, carbamazepine, rifampin, rifabutin, rifapentin, phenobarbital, St. John's Wort).
11. Participant has had a prior or concomitant non-VHL-associated malignancy with the exception of adequately treated basal or squamous cell carcinoma of the skin or any other malignancy from which the patient has remained disease free for more than five years.
12. Participant has had chemotherapy or radiotherapy within four weeks (six weeks for nitrosoureas or mitomycin C) prior to entering the study or those who have not recovered from adverse events (to Grade 1 or less toxicity according to CTCAE 3.0) due to agents administered more than four weeks earlier.
13. Participant is receiving other investigational agents.
14. Participants with known brain metastases (except when adequately controlled, i.e., have not grown in size, for ≥ 6 months before enrollment), not including hemangioblastoma, a known VHL complication of the brain.
15. Participant has a known bleeding disorder.
16. Participant is currently taking sunitinib malate or has taken sunitinib malate in the past.
Minimum Eligible Age
18 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
National Eye Institute (NEI)
NIH
Sponsor Role
lead
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
Responsibility Role
SPONSOR
Principal Investigators
Learn about the lead researchers overseeing the trial and their institutional affiliations.
Catherine Meyerle, MD
Role: PRINCIPAL_INVESTIGATOR
NEI/NIH
Locations
Explore where the study is taking place and check the recruitment status at each participating site.
National Institutes of Health Clinical Center, 9000 Rockville Pike
Bethesda, Maryland, United States
Site Status
Countries
Review the countries where the study has at least one active or historical site.
United States
References
Explore related publications, articles, or registry entries linked to this study.
Siemeister G, Weindel K, Mohrs K, Barleon B, Martiny-Baron G, Marme D. Reversion of deregulated expression of vascular endothelial growth factor in human renal carcinoma cells by von Hippel-Lindau tumor suppressor protein. Cancer Res. 1996 May 15;56(10):2299-301.
Reference Type
BACKGROUND
Iliopoulos O, Levy AP, Jiang C, Kaelin WG Jr, Goldberg MA. Negative regulation of hypoxia-inducible genes by the von Hippel-Lindau protein. Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10595-9. doi: 10.1073/pnas.93.20.10595.
Reference Type
BACKGROUND
Gnarra JR, Zhou S, Merrill MJ, Wagner JR, Krumm A, Papavassiliou E, Oldfield EH, Klausner RD, Linehan WM. Post-transcriptional regulation of vascular endothelial growth factor mRNA by the product of the VHL tumor suppressor gene. Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10589-94. doi: 10.1073/pnas.93.20.10589.
Reference Type
BACKGROUND
Dahr SS, Cusick M, Rodriguez-Coleman H, Srivastava SK, Thompson DJ, Linehan WM, Ferris FL 3rd, Chew EY. Intravitreal anti-vascular endothelial growth factor therapy with pegaptanib for advanced von Hippel-Lindau disease of the retina. Retina. 2007 Feb;27(2):150-8. doi: 10.1097/IAE.0b013e318030a290.
Reference Type
BACKGROUND
Kurban G, Hudon V, Duplan E, Ohh M, Pause A. Characterization of a von Hippel Lindau pathway involved in extracellular matrix remodeling, cell invasion, and angiogenesis. Cancer Res. 2006 Feb 1;66(3):1313-9. doi: 10.1158/0008-5472.CAN-05-2560.
Reference Type
BACKGROUND
Aiello LP, George DJ, Cahill MT, Wong JS, Cavallerano J, Hannah AL, Kaelin WG Jr. Rapid and durable recovery of visual function in a patient with von hippel-lindau syndrome after systemic therapy with vascular endothelial growth factor receptor inhibitor su5416. Ophthalmology. 2002 Sep;109(9):1745-51. doi: 10.1016/s0161-6420(02)01159-4.
Reference Type
BACKGROUND
Girmens JF, Erginay A, Massin P, Scigalla P, Gaudric A, Richard S. Treatment of von Hippel-Lindau retinal hemangioblastoma by the vascular endothelial growth factor receptor inhibitor SU5416 is more effective for associated macular edema than for hemangioblastomas. Am J Ophthalmol. 2003 Jul;136(1):194-6. doi: 10.1016/s0002-9394(03)00101-6.
Reference Type
BACKGROUND
Seizinger BR, Rouleau GA, Ozelius LJ, Lane AH, Farmer GE, Lamiell JM, Haines J, Yuen JW, Collins D, Majoor-Krakauer D, et al. Von Hippel-Lindau disease maps to the region of chromosome 3 associated with renal cell carcinoma. Nature. 1988 Mar 17;332(6161):268-9. doi: 10.1038/332268a0.
Reference Type
BACKGROUND
Maher ER, Bentley E, Yates JR, Latif F, Lerman M, Zbar B, Affara NA, Ferguson-Smith MA. Mapping of the von Hippel-Lindau disease locus to a small region of chromosome 3p by genetic linkage analysis. Genomics. 1991 Aug;10(4):957-60. doi: 10.1016/0888-7543(91)90185-h.
Reference Type
BACKGROUND
MELMON KL, ROSEN SW. LINDAU'S DISEASE. REVIEW OF THE LITERATURE AND STUDY OF A LARGE KINDRED. Am J Med. 1964 Apr;36:595-617. doi: 10.1016/0002-9343(64)90107-x. No abstract available.
Reference Type
BACKGROUND
Horton WA, Wong V, Eldridge R. Von Hippel-Lindau disease: clinical and pathological manifestations in nine families with 50 affected members. Arch Intern Med. 1976 Jul;136(7):769-77. doi: 10.1001/archinte.136.7.769.
Reference Type
BACKGROUND
Hardwig P, Robertson DM. von Hippel-Lindau disease: a familial, often lethal, multi-system phakomatosis. Ophthalmology. 1984 Mar;91(3):263-70. doi: 10.1016/s0161-6420(84)34304-4.
Reference Type
BACKGROUND
Green JS, Bowmer MI, Johnson GJ. Von Hippel-Lindau disease in a Newfoundland kindred. CMAJ. 1986 Jan 15;134(2):133-8, 146.
Reference Type
BACKGROUND
Ridley M, Green J, Johnson G. Retinal angiomatosis: the ocular manifestations of von Hippel-Lindau disease. Can J Ophthalmol. 1986 Dec;21(7):276-83.
Reference Type
BACKGROUND
Lamiell JM, Salazar FG, Hsia YE. von Hippel-Lindau disease affecting 43 members of a single kindred. Medicine (Baltimore). 1989 Jan;68(1):1-29. doi: 10.1097/00005792-198901000-00001.
Reference Type
BACKGROUND
Maher ER, Yates JR, Harries R, Benjamin C, Harris R, Moore AT, Ferguson-Smith MA. Clinical features and natural history of von Hippel-Lindau disease. Q J Med. 1990 Nov;77(283):1151-63. doi: 10.1093/qjmed/77.2.1151.
Reference Type
BACKGROUND
McDonald HR, Schatz H, Johnson RN, Abrams GW, Brown GC, Brucker AJ, Han DP, Lewis H, Mieler WF, Meyers S. Vitrectomy in eyes with peripheral retinal angioma associated with traction macular detachment. Ophthalmology. 1996 Feb;103(2):329-35 ; discussion 334-5. doi: 10.1016/s0161-6420(96)30696-9.
Reference Type
BACKGROUND
Kaelin WG Jr. Molecular basis of the VHL hereditary cancer syndrome. Nat Rev Cancer. 2002 Sep;2(9):673-82. doi: 10.1038/nrc885.
Reference Type
BACKGROUND
Rosenblatt MI, Azar DT. Anti-angiogenic therapy: Prospects for treatment of ocular tumors. Semin Ophthalmol. 2006 Jul-Sep;21(3):151-60. doi: 10.1080/08820530500350787.
Reference Type
BACKGROUND
Alvarez RH, Kantarjian HM, Cortes JE. Biology of platelet-derived growth factor and its involvement in disease. Mayo Clin Proc. 2006 Sep;81(9):1241-57. doi: 10.4065/81.9.1241.
Reference Type
BACKGROUND
Guo P, Hu B, Gu W, Xu L, Wang D, Huang HJ, Cavenee WK, Cheng SY. Platelet-derived growth factor-B enhances glioma angiogenesis by stimulating vascular endothelial growth factor expression in tumor endothelia and by promoting pericyte recruitment. Am J Pathol. 2003 Apr;162(4):1083-93. doi: 10.1016/S0002-9440(10)63905-3.
Reference Type
BACKGROUND
Morabito A, De Maio E, Di Maio M, Normanno N, Perrone F. Tyrosine kinase inhibitors of vascular endothelial growth factor receptors in clinical trials: current status and future directions. Oncologist. 2006 Jul-Aug;11(7):753-64. doi: 10.1634/theoncologist.11-7-753.
Reference Type
BACKGROUND
Mendel DB, Laird AD, Xin X, Louie SG, Christensen JG, Li G, Schreck RE, Abrams TJ, Ngai TJ, Lee LB, Murray LJ, Carver J, Chan E, Moss KG, Haznedar JO, Sukbuntherng J, Blake RA, Sun L, Tang C, Miller T, Shirazian S, McMahon G, Cherrington JM. In vivo antitumor activity of SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor and platelet-derived growth factor receptors: determination of a pharmacokinetic/pharmacodynamic relationship. Clin Cancer Res. 2003 Jan;9(1):327-37.
Reference Type
BACKGROUND
Motzer RJ, Michaelson MD, Redman BG, Hudes GR, Wilding G, Figlin RA, Ginsberg MS, Kim ST, Baum CM, DePrimo SE, Li JZ, Bello CL, Theuer CP, George DJ, Rini BI. Activity of SU11248, a multitargeted inhibitor of vascular endothelial growth factor receptor and platelet-derived growth factor receptor, in patients with metastatic renal cell carcinoma. J Clin Oncol. 2006 Jan 1;24(1):16-24. doi: 10.1200/JCO.2005.02.2574. Epub 2005 Dec 5.
Reference Type
BACKGROUND
O'Farrell AM, Foran JM, Fiedler W, Serve H, Paquette RL, Cooper MA, Yuen HA, Louie SG, Kim H, Nicholas S, Heinrich MC, Berdel WE, Bello C, Jacobs M, Scigalla P, Manning WC, Kelsey S, Cherrington JM. An innovative phase I clinical study demonstrates inhibition of FLT3 phosphorylation by SU11248 in acute myeloid leukemia patients. Clin Cancer Res. 2003 Nov 15;9(15):5465-76.
Reference Type
BACKGROUND
Abrams TJ, Murray LJ, Pesenti E, Holway VW, Colombo T, Lee LB, Cherrington JM, Pryer NK. Preclinical evaluation of the tyrosine kinase inhibitor SU11248 as a single agent and in combination with "standard of care" therapeutic agents for the treatment of breast cancer. Mol Cancer Ther. 2003 Oct;2(10):1011-21.
Reference Type
BACKGROUND
Murray LJ, Abrams TJ, Long KR, Ngai TJ, Olson LM, Hong W, Keast PK, Brassard JA, O'Farrell AM, Cherrington JM, Pryer NK. SU11248 inhibits tumor growth and CSF-1R-dependent osteolysis in an experimental breast cancer bone metastasis model. Clin Exp Metastasis. 2003;20(8):757-66. doi: 10.1023/b:clin.0000006873.65590.68.
Reference Type
BACKGROUND
Sakamoto KM. Su-11248 Sugen. Curr Opin Investig Drugs. 2004 Dec;5(12):1329-39.
Reference Type
BACKGROUND
Abrams TJ, Lee LB, Murray LJ, Pryer NK, Cherrington JM. SU11248 inhibits KIT and platelet-derived growth factor receptor beta in preclinical models of human small cell lung cancer. Mol Cancer Ther. 2003 May;2(5):471-8.
Reference Type
BACKGROUND
Schueneman AJ, Himmelfarb E, Geng L, Tan J, Donnelly E, Mendel D, McMahon G, Hallahan DE. SU11248 maintenance therapy prevents tumor regrowth after fractionated irradiation of murine tumor models. Cancer Res. 2003 Jul 15;63(14):4009-16.
Reference Type
BACKGROUND
Faivre S, Delbaldo C, Vera K, Robert C, Lozahic S, Lassau N, Bello C, Deprimo S, Brega N, Massimini G, Armand JP, Scigalla P, Raymond E. Safety, pharmacokinetic, and antitumor activity of SU11248, a novel oral multitarget tyrosine kinase inhibitor, in patients with cancer. J Clin Oncol. 2006 Jan 1;24(1):25-35. doi: 10.1200/JCO.2005.02.2194. Epub 2005 Nov 28.
Reference Type
BACKGROUND
Motzer RJ, Rini BI, Bukowski RM, Curti BD, George DJ, Hudes GR, Redman BG, Margolin KA, Merchan JR, Wilding G, Ginsberg MS, Bacik J, Kim ST, Baum CM, Michaelson MD. Sunitinib in patients with metastatic renal cell carcinoma. JAMA. 2006 Jun 7;295(21):2516-24. doi: 10.1001/jama.295.21.2516.
Reference Type
BACKGROUND
Bello CL, Sherman L, Zhou J, Verkh L, Smeraglia J, Mount J, Klamerus KJ. Effect of food on the pharmacokinetics of sunitinib malate (SU11248), a multi-targeted receptor tyrosine kinase inhibitor: results from a phase I study in healthy subjects. Anticancer Drugs. 2006 Mar;17(3):353-8. doi: 10.1097/00001813-200603000-00015.
Reference Type
BACKGROUND
Motzer RJ, Hoosen S, Bello CL, Christensen JG. Sunitinib malate for the treatment of solid tumours: a review of current clinical data. Expert Opin Investig Drugs. 2006 May;15(5):553-61. doi: 10.1517/13543784.15.5.553.
Reference Type
BACKGROUND
Escudier B, Chevreau C, Lasset C, Douillard JY, Ravaud A, Fabbro M, Caty A, Rossi JF, Viens P, Bergerat JP, Savary J, Negrier S. Cytokines in metastatic renal cell carcinoma: is it useful to switch to interleukin-2 or interferon after failure of a first treatment? Groupe Francais d'Immunotherape. J Clin Oncol. 1999 Jul;17(7):2039-43. doi: 10.1200/JCO.1999.17.7.2039.
Reference Type
BACKGROUND
Motzer RJ, Hutson TE, Tomczak P, Michaelson MD, Bukowski RM, Rixe O, Oudard S, Negrier S, Szczylik C, Kim ST, Chen I, Bycott PW, Baum CM, Figlin RA. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med. 2007 Jan 11;356(2):115-24. doi: 10.1056/NEJMoa065044.
Reference Type
BACKGROUND
Corless CL, McGreevey L, Town A, Schroeder A, Bainbridge T, Harrell P, Fletcher JA, Heinrich MC. KIT gene deletions at the intron 10-exon 11 boundary in GI stromal tumors. J Mol Diagn. 2004 Nov;6(4):366-70. doi: 10.1016/S1525-1578(10)60533-8.
Reference Type
BACKGROUND
Heinrich MC, Corless CL, Demetri GD, Blanke CD, von Mehren M, Joensuu H, McGreevey LS, Chen CJ, Van den Abbeele AD, Druker BJ, Kiese B, Eisenberg B, Roberts PJ, Singer S, Fletcher CD, Silberman S, Dimitrijevic S, Fletcher JA. Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. J Clin Oncol. 2003 Dec 1;21(23):4342-9. doi: 10.1200/JCO.2003.04.190.
Reference Type
BACKGROUND
Blanke CD, Corless CL. State-of-the art therapy for gastrointestinal stromal tumors. Cancer Invest. 2005;23(3):274-80. doi: 10.1081/cnv-200055972.
Reference Type
BACKGROUND
Van Glabbeke M, Verweij J, Casali PG, Le Cesne A, Hohenberger P, Ray-Coquard I, Schlemmer M, van Oosterom AT, Goldstein D, Sciot R, Hogendoorn PC, Brown M, Bertulli R, Judson IR. Initial and late resistance to imatinib in advanced gastrointestinal stromal tumors are predicted by different prognostic factors: a European Organisation for Research and Treatment of Cancer-Italian Sarcoma Group-Australasian Gastrointestinal Trials Group study. J Clin Oncol. 2005 Aug 20;23(24):5795-804. doi: 10.1200/JCO.2005.11.601.
Reference Type
BACKGROUND
Patyna S, Peng G. Distribution of sunitinib and its active metabolite in brain and spinal cord tissue following oral or intravenous administration in rodents and monkeys. European Journal of Cancer Suppl 4(12):21(Abstract 56), 2006.
Reference Type
BACKGROUND
http://www.rxlist.com/cgi/generic/sutent
Reference Type
BACKGROUND
http://www.pfizer/download/uspi_sutent.pdf
Reference Type
BACKGROUND
http://ctep.cancer.gov/forms/CTCAEv3.pdf
Reference Type
BACKGROUND
http://ctep.cancer.gov/guidelines/recist.html
Reference Type
BACKGROUND
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
08-EI-0129
Identifier Type: OTHER
Identifier Source: secondary_id
080129
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.
A Study to Learn How Well Aflibercept Injected Into the Eye Works and How Safe it is When Given in Customized Treatment Intervals in Patients With an Eye Disease Called Neovascular Age-related Macular Degeneration After Start of Treatment
NCT05473715
TERMINATED
PHASE4
A Study to Assess the Safety, Tolerability and Effectiveness of MT-0814 for the Treatment of Age-related Macular Degeneration
NCT03869684
TERMINATED
PHASE2
Study of the Effects of High Dose Aflibercept Injected Into the Eye of Patients With an Age-related Disorder That Causes Loss of Vision Due to Growth of Abnormal Blood Vessels at the Back of the Eye
NCT04423718
COMPLETED
PHASE3
Phase II/III Study of Anti-VEGF in Neovascular AMD
NCT00021736
COMPLETED
PHASE2/PHASE3
A Study to Learn How Avacincaptad Pegol (Izervay™) is Used in Clinical Practice in People Who Have Geographic Atrophy
NCT06779773
RECRUITING
Study of MP0112 Intravitreal Injection in Patients With Wet Age Related Macular Degeneration
NCT01086761
TERMINATED
PHASE1
Intravitreal Aflibercept Injection for the Treatment of Submacular Vascularized Pigment Epithelial Detachment
NCT01722656
COMPLETED
PHASE4
A Study of Encapsulated Cell Technology (ECT) Implant for Participants With Early Stage Retinitis Pigmentosa
NCT00447980
COMPLETED
PHASE2
Adjunctive Photodynamic Therapy + Aflibercept vs. Afilbercept Alone for PDA in NV AMD
NCT02457026
WITHDRAWN
NA
Intravitreal Aflibercept for Submacular Hemorrhage
NCT03169660
COMPLETED
PHASE4
Assessment of Proactive Treatments in Patients With Wet Age-related Macular Degeneration (wAMD) Which Have Never Undergone Treatment of This Particular Disease
NCT03939767
COMPLETED
Sirolimus Versus Anti-Vascular Endothelial Growth Factor (antiVEGF) for Wet AMD
NCT02357342
COMPLETED
PHASE2
Effect Aflibercept on Ocular Perfusion
NCT03804099
COMPLETED
PHASE4
Treatment of Age-Related Macular Degeneration With Anecortave Acetate
NCT00211458
COMPLETED
PHASE2
Safety and Efficacy of ADVM-022 in Treatment-Experienced Patients With Neovascular Age-related Macular Degeneration [LUNA]
NCT05536973
ACTIVE_NOT_RECRUITING
PHASE2
Vascular Endothelial Growth Factor (VEGF) Trap-Eye: Investigation of Efficacy and Safety in Wet Age-Related Macular Degeneration (AMD)
NCT00637377
COMPLETED
PHASE3
A Depot Formulation of Sunitinib Malate (GB-102) Compared to Aflibercept in Subjects With Wet AMD
NCT03953079
COMPLETED
PHASE2
A Study of Implantation of Retinal Pigment Epithelium in Subjects with Acute Wet Age Related Macular Degeneration
NCT01691261
COMPLETED
PHASE1
Short-term Clinical Effects of Intravitreal Aflibercept Injection 2.0mg as a Predictor of Long-term Results
NCT01657669
UNKNOWN
PHASE4
Aflibercept After Ranibizumab in Exudative Age-related Macular Degeneration
NCT02157077
COMPLETED
PHASE3
A Study Testing if Medicine Can Make Pigment Epithelium Detachments Regress and Stabilize the Vision in Eyes
NCT01746875
TERMINATED
NA
Intravitreal Injections of rhuFab V2 in Combination With Visudyne in Subjects With Age Related Macular Degeneration (AMD)
NCT00056823
COMPLETED
PHASE1/PHASE2
Intravitreous Pegaptanib Sodium Injection in Patients With Exudative Age-Related Macular Degeneration (AMD)
NCT00088192
COMPLETED
NA
A Study to Comparing SCD411 and Eylea® in Subjects With Wet Age-related Macular Degeneration (AMD)
NCT04480463
COMPLETED
PHASE3