The Controlled Trial of Apremilast for Rheumatoid Arthritis Treatment (CARAT)
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|ClinicalTrials.gov Identifier: NCT01250548|
Recruitment Status : Completed
First Posted : December 1, 2010
Last Update Posted : September 3, 2014
The purpose of this study is to compare the effects of apremilast with a placebo (an inactive substance that looks like apremilast) on you and other people with rheumatoid arthritis.
The investigators will be collecting information in this study to help us determine -
- the safety of apremilast in patients with active rheumatoid arthritis
- how long it takes for patients with active rheumatoid arthritis to respond to apremilast
- how long the effects of apremilast last after the treatment has ended.
|Condition or disease||Intervention/treatment||Phase|
|Rheumatoid Arthritis||Biological: apremilast Other: Placebo||Phase 2|
Many manifestations associated with RA result from, or are significantly influenced by, the effects of pro-inflammatory cytokines (e.g., TNF, IL-1, IL-6). Specific inhibition of these cytokines with newer, parenterally administered biologic agents has revolutionized the treatment of RA. Apremilast is a novel, orally administered drug which approaches the reduction of pro-inflammatory cytokines via inhibition of phosphodiesterase type 4 (PDE4).
Apremilast, Acetamide, N-[2-[ (1S)-1-(3-ethoxy-4-methoxyphenyl)-2-(methylsulfonyl) ethyl]-2,3-dihydro-1,3-dioxo-1H-isoindol-4-yl] is a phosphodiesterase type 4 (PDE4) inhibitor under development for use in the treatment of inflammatory conditions.
PDE4 is one of the major phosphodiesterases expressed in leukocytes. Inhibitors of PDE4 cause accumulation of intracellular cyclic adenosine monophosphate (cAMP), which in turn activates protein kinase A and other downstream effectors, resulting in inhibition of pro-inflammatory cytokine transcription and other cellular responses such as neutrophil degranulation, chemotaxis, and adhesion to endothelial cells.
In human cellular models, apremilast inhibited production of inflammatory mediators such as TNF-α, IL-12, IL-2, IFN-γ, IL-5, IL-8, leukotriene B4 (LTB4), and the adhesion molecule CD18/CD11b (Mac-1).
Apremilast has also been shown to be a potent anti-inflammatory agent in several animal models of inflammation.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||34 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Double (Participant, Investigator)|
|Official Title:||The Controlled Trial of Apremilast for Rheumatoid Arthritis Treatment|
|Study Start Date :||May 2010|
|Actual Primary Completion Date :||June 2014|
|Actual Study Completion Date :||June 2014|
|Active Comparator: 2||
30 mg BID apremilast taken orally for the first 12 weeks followed by responders randomized to either 30 mg BID apremilast (oral) or 30 mg BID placebo (oral) for 8 weeks
Placebo Comparator: Apremilast
Placebo Compared to apremilast arm
- To determine the time to response for subjects with active RA taking apremilast (30 mg per os [PO], twice per day [BID]) [ Time Frame: 1.5 years ]
- Determine time to flare when apremilast is withdrawn [ Time Frame: 1.5 years ]
- Assess the efficacy and magnitude of response to apremilast in active RA measured by ACR 20, 50, & 70 response rates [ Time Frame: 2 years ]
- Assess safety of apremilast in subjects with active RA [ Time Frame: 2 years ]Review of labs and possible adverse effects of study drug including Data Safety Monitoring Committee analysis.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01250548
|United States, Texas|
|Baylor Research Institute - Arthritis Care and Research Center|
|Dallas, Texas, United States, 75231|
|Principal Investigator:||John Cush, MD||Baylor Research Institute|