pSivida Corp. (NSDQ:PSDV) is touting a study of a drug-device combination that it says helps slow the advance of a degenerative eye disease called retinitis pigmentosa.
The disease involves the gradual deterioration of the rods and cones that make up the retina. Symptoms begin with night blindness and progress over years or decades to tunnel vision and, often, total blindness. CEO Dr. Paul Ashton told MassDevice that the Watertown, Mass.-based company’s Durasert is inserted into the back of the eye, where it slowly releases a steroid called fluocinolone acetonide.
"It’s a truly horrible disease," Ashton told us, speaking on his cell phone outside a pub in his native England. "Typically, people get diagnosed in about their 30s and you’re normally totally blind by the time you’re 50. It’s completely untreatable."
Retinitis pigmentosa occurs when the byproducts of normal vision accumulate, he explained.
"Basically, whenever you process a visual image, the rods and cones produce a lot of by-products which, in a normal cell, get cleared. In retinitis pigmentosa, they accumulate. That’s what eventually kills the cells and the lights go out. What we’ve done is use a very small insertable drug delivery device to release a steroid directly into the eye that will just provide some protection and slow down the rates of vision loss. With a condition that takes 20 years to make you blind, if you slow it down by a factor of two, that’s pretty good."
The study, published in the journal Investigative Ophthalmology and Visual Science, showed that the Durasert device slowed the disease’s progression in rats. The researchers used electroretinography, which measures the electrical response of the rods and cones to light, to chart the effectiveness of the device compared with rats with no device inserted or with a device inserted that contained no steroids.
"The animals that received these implants had preserved vision. The retina, kind of like the camera film, the structure or architecture of the retina was preserved. Normally it goes to hell pretty quick," Ashton said. "In a rat with retinitis pigmentosa, that ‘blip’ [on the ERG] gets pretty flat pretty quick and eventually flat-lines. We found that those pulses on the ERG were preserved significantly longer in eyes that were receiving implants."
The study showed that the rats with no implants or with the dummy implants suffered a 50 percent to 60 percent reduction in ERG amplitudes four weeks after implantation. Two other groups of rats each received implants containing the FA steroid, one of which received a higher dose. The rats with the lower dose showed a 15 percent rate of amplitude attenuation, while the higher-dose rates showed a 30 percent reduction.
Ashton said pSivida is developing a larger implant for humans, aimed at treating diabetic eye disease, that’s in clinical trials now. The company is also working on a treatment for macular edema, he said.
"These devices release drugs very, very slowly. In the human trial, you’re looking at devices designed to last for up to three years from a single insertion. The idea is to maintain low therapeutic [drug] levels over a long period of time. Eye diseases are difficult, because eye drops only get to the front of the eye. It’s very difficult to get drugs to the back of the eye, the retina, which is where all the damage occurs," Ashton said. "The technology can be used virtually anywhere. If something is small enough and safe enough to be injected into the eye, it can be used anywhere — brains, organs, anywhere."