AAAAI: Third Time a Charm for Novel HAE Drug

by Symptom Advice on March 23, 2011

SAN FRANCISCO — Hereditary angioedema attacks resolve faster with the novel agent icatibant (Firazyr), according to a clinical trial designed to answer FDA doubts over its efficacy in the wake of conflicting results from two pivotal studies. In the multinational trial, icatibant cut median time to clinically significant relief from acute swelling and pain to 2.0 hours compared with 19.8 hours on placebo (P<0.001), William R. Lumry, MD, of the University of Texas Southwestern Medical Center in Dallas, and colleagues found. Composite visual analog symptom scores continued to drop over the first four hours and remained significantly lower compared with placebo at every point through 12 hours, Lumry’s group reported here at the American Academy of Allergy, Asthma & Immunology meeting. the FDA rejected the drug in 2008 over disappointing results from the two key phase III trials of icatibant.Action Points  

  • Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
  • Note that in this study icatibant, a selective bradykinin beta-2 receptor antagonist, relieved symptoms in attacks of acute hereditary angioedema significantly faster than placebo.
  • Point out that the drug is investigational and has not been approved by the FDA, in part due to less than significant results in prior studies.

The first trial, FAST-1, showed no advantage over placebo in the same endpoint of time to relief of acute angioedema attacks.

FAST-2 did show an advantage over the active comparator tranexamic acid, but this was likely due to the low use of rescue medications that made the comparator look worse than placebo in FAST-1.

The third trial in the series, sponsored by German drugmaker Jerini in response to the FDA’s concerns, was seen as good news by Lumry, who played up the drug as “much more effective” than placebo.

Until recently, the only treatment option for the rare genetic disorder that causes frequent attacks of painful swelling in various parts of the body were straight replacements for the defective protein derived from human plasma.

Within the past two years, a synthetic option became available to treat acute attacks, the drug ecallantide (Kalbitor) that targets the main chemical that causes the swelling, bradykinin.

Icatibant, which blocks the same bradykinin pathway in a different way, could be useful as another synthetic option, Lumry suggested.

“This is a unique action type of a product and hopefully it will add to the things we can do to treat this population,” he told MedPage Today.

The FAST-3 trial randomized 98 adult patients in 11 countries to double-blind treatment with a single subcutaneous injection of icatibant (3 ml) or saline placebo within 12 hours of the onset of a moderate to very severe swelling attack of Type I or II hereditary angioedema.

The trial included cutaneous, abdominal, and laryngeal sites of swelling, so severe laryngeal cases were given open-label icatibant immediately to protect their airway.

Among the secondary endpoints for the nonlaryngeal intent-to-treat population, the researchers showed that icatibant was faster than placebo for the following:

  • Time to initial symptom relief (0.8 versus 3.5 hours, P<0.001)
  • Time to onset of primary symptom relief (1.5 versus 18.5 hours, P<0.001)
  • Time to “almost complete” symptom relief (8.0 to 36.0 hours, P=0.012)

The 10 laryngeal cases treated in the study tended to show faster relief with icatibant as well.

Rescue therapy, a concern in the prior trials, was allowed but withheld, if possible, until eight or nine hours after study drug injection.

In the nonlaryngeal population, 35.6% of placebo-group patients got rescue medications prior to onset of symptom relief — and a total of 40.0% got them at any point during the attack through the five days after treatment compared with 7.0% in the icatibant group (P<0.001).

In the laryngeal population, half of the patients who got placebo needed rescue medications and one of the double-blind icatibant group patients (33.3%) did as well through five days post-treatment.

These rates were much higher than the criticized 20% rate of rescue therapy use in the active comparator group of FAST-2 and more on par with the 45% who got it within the first 12 hours in the placebo group of FAST-1.

Adverse events overall occurred less often with icatibant in FAST-3 (41% versus 52% placebo), although all icatibant-treated patients experienced some type of transient injection site reaction.

The drug was not associated with any serious adverse events, but drug-related adverse events were one case each of diarrhea, nausea, dyspepsia, headache, and injection site erythema. Laboratory and vital signs remained unaffected by icatibant.

No cases of the hypersensitivity or anaphylactic reactions seen in some cases with ecallantide were mentioned in the FAST-3 presentation, and Lumry noted that none of the patients tested positive for antibodies to icatibant.

Head-to-head comparisons with other acute treatments for hereditary angioedema attacks have yet to be done, and comparison is difficult due to the different endpoints used to assess symptom relief, he noted.

In the FAST trials, this primary endpoint was time to a clinically significant 50% reduction in visual analog symptom score from baseline whereas others used measures such at improvement at four hours.

But, “we’ve looked at this data and the on-demand therapies all seem to work in the same time frame, in about one to two hours,” he told attendees at the session.

The study was sponsored by Jerini in collaboration with Shire Human Genetic Therapies.

Lumry reported conflicts of interest with Alcon Laboratories, AstraZeneca, Boehringer Ingelheim, CSL Behring, Dyax, Genentech, GlaxoSmithKline, Meda, Merck, Novartis, sanofi-aventis, Shire, Viropharma, Teva, Pfizer, Sepracor, Biotest, and UCB Pharmaceuticals.

Two co-authors reported employment with Shire Human Genetic Therapies.

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