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1 higher rate of injection-site reactions with alirocumab.
2 on in the rate of cardiovascular events with alirocumab.
3 analysis included 4974 patients (3182 taking alirocumab, 1174 taking placebo, 618 taking ezetimibe).
4 domized placebo-phase, double-blind study of alirocumab 150 mg administered subcutaneously every 2 we
5  randomly assigned in a 2:1 ratio to receive alirocumab (150 mg) or placebo as a 1-ml subcutaneous in
6 5 mg (a PCSK9 inhibitor); and uptitration to alirocumab, 150 mg.
7 eeks apart, followed by 5 doses of 150 mg of alirocumab, 2 weeks apart.
8 ge LDL-C <50 mg/dL (44.7%-52.6% allocated to alirocumab, 6.5% allocated to ezetimibe, and 0% allocate
9                         Randomization was to alirocumab 75/150 mg every 2 weeks or control for 24 to
10                                              Alirocumab, a monoclonal antibody that inhibits proprote
11                                              Alirocumab, a monoclonal antibody to proprotein converta
12                                              Alirocumab, a PCSK9 antibody, markedly lowers LDL-C leve
13 holesale acquisition costs of evolocumab and alirocumab); adopted a health-system perspective, lifeti
14 taract incidence was observed between pooled alirocumab and control groups.
15                                              Alirocumab and evolocumab are monoclonal antibodies that
16                                              Alirocumab and evolocumab are monoclonal antibodies that
17       At week 24, the difference between the alirocumab and placebo groups in the mean percentage cha
18 nce of cardiovascular benefit for ezetimibe, alirocumab, and evolocumab positions these drugs as add-
19  [placebo or ezetimibe]; representing 4,029 [alirocumab] and 2,114 [control] double-blind patient-yea
20                                              Alirocumab decreased LDL-C and LDL-apoB by increasing ID
21  background statin (n = 4629) were pooled by alirocumab dose (75 or 150 mg every 2 weeks) and control
22                                          The alirocumab group, as compared with the placebo group, ha
23                                              Alirocumab had no effects on FCRs or PRs of very low-den
24 mechanistic studies of the Lp(a) lowering by alirocumab in humans have been published to date.
25 eductions with the PCSK9 monoclonal antibody alirocumab may be affected by background statin dose due
26 tation patients randomly assigned to receive alirocumab, mean percent reduction in LDL-C at 2 weeks w
27 le-blind treatment 8 to 104 weeks; n = 3,340 alirocumab, n = 1,894 control [placebo or ezetimibe]; re
28                                  In summary, alirocumab provided consistent LDL-C reductions and was
29                                              Alirocumab reduced ultracentrifugally isolated LDL-C by
30 na requiring hospitalization) was lower with alirocumab than with placebo (1.7% vs. 3.3%; hazard rati
31 tin, 80 mg; add-on ezetimibe therapy; add-on alirocumab therapy, 75 mg (a PCSK9 inhibitor); and uptit
32                                           In alirocumab-treated patients, 839 (25.1%) achieved 2 cons
33            The increase in apo(a) FCR during alirocumab treatment suggests that increased LDL recepto
34       After all subjects received 8 weeks of alirocumab treatment, LDL-C was reduced by 73% from base
35 atients achieving LDL-C goals at Week 24 for alirocumab versus control (interaction P-values non-sign
36  Incidence of adverse events was similar for alirocumab versus control, except for a higher rate of i
37                                The safety of alirocumab was evaluated in patients with at least 2 con
38             LDL-C levels <25 or <15 mg/dl on alirocumab were not associated with an increase in overa
39                   Over a period of 78 weeks, alirocumab, when added to statin therapy at the maximum
40 ents within the ODYSSEY trials that compared alirocumab with controls (placebo/ezetimibe), mainly as

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