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news.Ark Therapeutics (Ark) has enrolled and treated the first patient in the phase I/IIa trial of adenoviral short-form Vascular Endothelial Growth Factor-D (VEGF-D), in patients with refractory angina. The trial is being undertaken in collaboration with the AI Virtanen Institute in Kuopio, Finland. The programme (EG011) uses the angiogenic VEGF-D?N?C short-form gene (Ad-VEGF-D).
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The company reported that the patient was given a single dose of 1 X 109 viral particles of Ad-VEGF-D and has been moved from post operative critical care recovery to the general ward. The NOGA catheter procedure to administer EG011 was uneventful and no adverse events of concern, beyond those expected in the standard surgical procedure, had been observed at the day 2 recovery point.
The phase I/IIa trial is an ascending dose controlled study in up to 30 chronic angina patients, who have already been treated unsuccessfully with available licensed approaches, usually stents and balloon angioplasty.
Patients will receive a single dose of either 1×109, 1×1010 or 1×1011 viral particles of Ad-VEGF-D, administered via the NOGA catheter system after NOGA mapping of the wall of the myocardium, to locate the ischaemic areas. Controls will receive only NOGA mapping and patients will be blinded to the treatment groups.
The study has been approved by the Finnish National Agency for Medicines (NAM) and is being conducted by Professor Yla-Herttuala of the AI Virtanen Institute in Kuopio, and Professor Juha Hartikainen and Doctor Marja Hedman of the Kuopio University Hospital. The study will assess the safety of EG011 as well as provide initial efficacy data.
Earlier in June 2008, in the second pre-clinical therapeutic proof-of-principle study, EG011 had demonstrated an ability to grow new blood vessels and restore heart function following a heart attack (myocardial infarction). EG011 induced a four-fold increase in capillaries, which were haemodynamically functional at 21 days. The amount of blood pumped from the ventricle, where the heart attack occurred, was restored from 60% to 90% of the level before the heart attack, a highly significant (p=0.0002) result. A non active ‘marker’ gene (lacZ) in the same adenoviral vector was used as a control.
EG011 appeared well tolerated with no differences in serious adverse events observed between active and control groups.