SP01A: The Study of an Oral Entry Inhibitor in Treatment-Experienced HIV Patients
|First Received Date ICMJE||March 3, 2006|
|Last Updated Date||October 25, 2006|
|Start Date ICMJE||March 2006|
|Primary Completion Date||Not Provided|
|Current Primary Outcome Measures ICMJE
||Within treatment group reduction in viral load (log10) in each SP01A active arm as well as within the placebo arm as measured from DAY-1 (Baseline) to DAY-22, and DAY-29 (Study-End).|
|Original Primary Outcome Measures ICMJE||Same as current|
|Change History||Complete list of historical versions of study NCT00299897 on ClinicalTrials.gov Archive Site|
|Current Secondary Outcome Measures ICMJE
||Reduction in viral load compared across SP01A active arms measured from DAY-1 (Baseline) to DAY-22 and DAY-29 (Study-End).|
|Original Secondary Outcome Measures ICMJE||Same as current|
|Current Other Outcome Measures ICMJE||Not Provided|
|Original Other Outcome Measures ICMJE||Not Provided|
|Brief Title ICMJE||SP01A: The Study of an Oral Entry Inhibitor in Treatment-Experienced HIV Patients|
|Official Title ICMJE||A Multi-Center, Double-Blind, Randomized, Placebo-Controlled Study of Orally Administered SP01A for 28 Days as Monotherapy Treatment in HIV-Infected Patients With Evidence of Resistance to Currently Available Antiretroviral Therapy|
This is a 28-day, multi-center, placebo-controlled study designed to look at the dose response, efficacy, and safety of SP01A, given as a pill to be swallowed, in the treatment of HIV-infected subjects.
Samaritan has discovered that SP01A affects cholesterol binding, which is directly implicated in the pathogenesis of HIV. It has also been established that drugs of this nature exert an anti-HIV effect in-vitro. These data suggest that SP01A has the potential to reduce HIV virus replication.
One measurement of an HIV infected person’s risk of progressing to AIDS is the number of viral particles of HIV in their blood (called a “viral load”). This study is designed to see if SP01A will lower the amount of HIV in an infected individual's blood. Patients will be assigned by chance to 1 of 4 groups. Neither the patient nor the study doctor or nurse will know which dose of the study drug the patient is taking or if he/she is receiving the placebo (a capsule that looks like the study drug but does not contain any active ingredient).
Study drug administration will continue for 28 days. At the end of the 28-day study, the patient will be offered testing of his/her virus for resistance to approved drugs (genotype).
Currently approved antiretroviral medications target either the HIV viral reverse transcriptase (RT), (Nucleoside Reverse Transcriptase Inhibitors (NRTIs) and Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)) or the viral protease, (Protease Inhibitors (PIs)) or inhibit viral fusion with target cells (Fusion Inhibitors). A regimen using a combination of these agents is considered the standard of care and, when effective, results in suppression of the virus below the detection limits.
However, the long-term use of antiretroviral therapy is sometimes hampered by poor compliance due to pill burden, food restrictions, and major side effects that impact Quality of Life. Furthermore, one of the major reasons for therapy failure is the emergence of resistant virus against one or more of the anti-HIV medications or, to some extent, an entire class of drug (cross resistance).
Enfuvirtide (Fuzeon™) was recently approved as an HIV-1 fusion/entry inhibitor, a new class of treatment that prevents fusion of the HIV-1 virus to the CD4+ cell membrane by preventing the conformational changes required for this fusion. Since the mechanism of action of Enfuvirtide is different from other classes of anti-HIV medication, it is effective in patients who have failed other therapies due to emergence of resistant virus. However, a recent study demonstrated the emergence of resistance to Enfuvirtide due to a mutation in viral gp41.
The rapid rate of mutation of HIV-1 and conferred resistance of the virus to current therapies continues to necessitate a need for additional therapeutic agents. To that end, a hypothesis has been suggested regarding the immuno-modulating and anti-viral effects of SP01A in the treatment of HIV infection.
SP01A may affect cholesterol binding, which is directly implicated in the pathogenesis of HIV. Several observations have also established that inhibitors of cholesterol synthesis inhibit cell fusion formation induced by HIV-l and that drugs extracting cholesterol from the cellular membrane exert an anti-HIV-1 effect in-vitro. Taken together, these data may suggest that procaine hydrochloride and SP01A reduces HIV-1 virus replication by modifying the cholesterol content of the cell membrane, rendering it much more difficult for the virus to enter and infect the cell.
There is an urgent need to develop improved new therapeutic agents. SP01A, which targets different viral or cellular components with a new mechanism of action, is being developed and tested by Samaritan Pharmaceuticals, Inc. as a new anti-viral therapeutic agent.
This multi-center, double-blind, randomized, placebo-controlled study of orally administered SP01A as monotherapy in HIV-infected patients with evidence of resistance to currently available antiretroviral therapy was designed to further evaluate the dose response, efficacy, and safety of SP01A. HIV-positive patients will be evaluated during the pre-study period. Following a 2-week washout period (if required), patients will be randomized into one of four study arms and all arms will initiate the 28-day monotherapy study. The first arm will receive 200 mg of SP01A QID. Arm Two will receive 200 mg bid. The third arm will orally administer 400 mg bid. Finally, the fourth arm will receive placebo twice daily.
During the treatment period, patients will make five scheduled visits to the treatment facility on or about Days 1, 8, 15, 22, and 29. During these visits patients will be monitored for viral load and general health parameters. At the conclusion of the 28-day monotherapy study, patients will have optimized viral testing for further treatment.
On Day 43, patients will make their final visit to the treatment facility for post-study evaluation.
|Study Type ICMJE||Interventional|
|Study Phase||Phase 2|
|Study Design ICMJE||Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Primary Purpose: Treatment
|Intervention ICMJE||Drug: SP01A|
|Study Arm (s)||Not Provided|
|Publications *||Xu J, Lecanu L, Han Z, Yao Z, Greeson J, Papadopoulos V. Inhibition of adrenal cortical steroid formation by procaine is mediated by reduction of the cAMP-induced 3-hydroxy-3-methylglutaryl-coenzyme A reductase messenger ribonucleic acid levels. J Pharmacol Exp Ther. 2003 Dec;307(3):1148-57.|
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
|Recruitment Status ICMJE||Active, not recruiting|
|Completion Date||Not Provided|
|Primary Completion Date||Not Provided|
|Eligibility Criteria ICMJE||
Prior to the first day of study drug:
Patients are ineligible to participate in the study if ANY of the following criteria are met.
|Ages||18 Years to 60 Years (Adult)|
|Accepts Healthy Volunteers||No|
|Contacts ICMJE||Contact information is only displayed when the study is recruiting subjects|
|Listed Location Countries ICMJE||United States|
|Removed Location Countries|
|NCT Number ICMJE||NCT00299897|
|Other Study ID Numbers ICMJE||SP01A-111-05|
|Has Data Monitoring Committee||Not Provided|
|Plan to Share Data||Not Provided|
|IPD Description||Not Provided|
|Responsible Party||Not Provided|
|Study Sponsor ICMJE||Samaritan Pharmaceuticals, Inc|
|Collaborators ICMJE||Not Provided|
|Information Provided By||Samaritan Pharmaceuticals, Inc|
|Verification Date||October 2006|
ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP