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David Freedman Medicine Professional Corporation

6633 Highway #7 East, Markham

Tel: 905.472.7127   email: Ashgrove@cardiomatters.com

398 Steeles Ave West, Thornhill

Tel: 905.881.0334  email: Steeles@cardiomatters.com

CANTOS 2017 august

Monclonal antibody Canakinumab

selectively inhibits the proinflammatory cytokine interleukin-1 beta (IL-1ß).

significantly decreased the risk of recurrent major CV events without any effect on cholesterol and, in a surprising twist, also dramatically cut rates of new lung cancer and lung-cancer mortality, 

10,000 high-risk patients who had a prior MI and persistently elevated high-sensitivity C-reactive protein (hs-CRP) levels, showed that patients who received subcutaneous canakinumab 150 mg every 3 months had a

15% reduced risk for the composite primary end point of nonfatal MI, nonfatal stroke, and CV death compared with those receiving placebo (P=0.02075).

Reduced the need for revascularization by about 30% (P<0.0001).

"This is the first time we have rock-solid evidence that in the absence of lowering cholesterol but by lowering inflammation, we have risk reductions that are substantial and in this case identical to what you get for lowering LDL. 

It actually significantly reducing the incidence of arthritis, osteoarthritis, gout, and fatal cancers.

Enthusiasm for the results may be tempered by a lack of effect on CV death in the trial and a significant increase in deaths due to infection with canakinumab vs placebo (incidence rate 0.31 vs 0.18 events per 100 person-years; P=0.02). These events happened relatively early on and were more likely in older patients with diabetes.Should canakinumab move forward in CVD, Ridker said patients will require monitoring for early signs and symptoms similar to what is done for patients taking biologic drugs.

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