US-based biopharmaceutical firm Dyax has started dosing patients in its Phase Ib clinical trial of DX-2930, an investigational fully human monoclonal antibody inhibitor of plasma kallikrein (pKal), for treatment of hereditary angioedema (HAE).

The trial is designed to assess the safety, tolerability, and pharmacokinetics of multiple subcutaneous administrations of DX-2930 in HAE patients.

DX-2930 is being developed by the company as a subcutaneous injection for prevention of HAE attacks.

Dyax executive vice-president of research and development and chief medical officer Burt Adelman said the primary purpose of the Phase Ib trial is to gain important safety and pharmacokinetic data in the target patient population.

“Data from this study will guide dosing decisions for future clinical development.”

“The pharmacodynamic effects of DX-2930 on plasma kallikrein will also be evaluated,” Adelman said. “Data from this study will guide dosing decisions for future clinical development.

“We’ll also be utilising our biomarker assay to assess the possible impact of DX-2930 on exploratory pharmacodynamic parameters such as basal plasma kallikrein activity.”

The company intends to report results of the multi-centre, randomised, double-blind, placebo-controlled, multiple ascending dose trial in early 2015.

A total of 18 patients will be enrolled into three ascending dose groups (30mg, 100mg and 300mg) of DX-2930 or placebo.

The company said that there will be four active drug-treated subjects and two placebo-treated subjects per group.

Each patient will receive two treatments with study drugs, separated by two weeks, and undergo 15 weeks of follow-up after the second dose.

Dyax president and CEO Gustav Christensen said data generated from the Phase Ib trial will provide the basis for the company to continue to advance DX-2930.

“We believe that, if approved, DX-2930 has the potential to be a game-changing therapy for HAE patients,” Christensen said.

According to the company, uncontrolled pKal activity leads to excessive generation of bradykinin, a vasodilator thought to be responsible for the localised swelling, inflammation and pain characteristically associated with HAE.

This disorder is caused by low or dysfunctional levels of C1 esterase inhibitor (C1-INH), a naturally occurring molecule that inhibits pKal, a key mediator of inflammation, and other serine proteases in the blood.