Protalex enrols first patient in cohort four of PRTX-100-202 Study

11th April 2018 (Last Updated April 11th, 2018 00:00)

Protalex has enrolled the first of three patients in the fourth cohort of its PRTX-100-202 Study, a Phase I/II trial of PRTX-100 for the treatment of adults with persistent/chronic Immune Thrombocytopenia (ITP).

Protalex has enrolled the first of three patients in the fourth cohort of its PRTX-100-202 Study, a Phase I/II trial of PRTX-100 for the treatment of adults with persistent/chronic Immune Thrombocytopenia (ITP).

Based in the US, the patient has already received 12mg/kg, which is double the dose used in the prior cohort of PRTX-100 6mg/kg.

The opening of the fourth cohort in the US and UK was carried out after a planned, interim analysis of safety and efficacy data received from cohort three.

"Opening additional clinical sites in the UK will facilitate increased enrolment, and support trial completion within the next several months."

The open-label, dose-escalation PRTX-100-202 study seeks to enrol patients in up to six cohorts.

During the study, patients will receive four weekly intravenous doses of PRTX-100 and are kept under observation for up to 48 weeks thereafter.

Its primary objective is a platelet response to PRTX-100, while secondary objectives include safety, immunogenicity, and pharmacokinetics.

The trial is currently enrolling patients at various clinical sites in the US and the UK.

Protalex ITP Programs vice-president Richard Francovitch said: “Opening additional clinical sites in the UK will facilitate increased enrolment, and support trial completion within the next several months.

“As noted previously, we are encouraged by the data collected in prior cohorts treated at lower doses. The ability to compare dosing outcomes at multiple levels will inform our next step for the development of PRTX-100.”

PRTX-100 has previously received orphan drug designation in the US and Europe for the treatment of ITP, an autoimmune condition characterised by bruising and increased bleeding due to immune-mediated accelerated destruction of platelets and impaired production of platelets.