The challenge in ophthalmologic degenerative disease is mostly not how to restore what has already been lost, but how to preserve what remains. That distinction is particularly important in conditions such as retinitis pigmentosa (RP), geographic atrophy and glaucoma, where progressive loss of retinal function can continue over many years and where treatment options remain limited.
One approach now moving from experimental concept towards a more defined clinical role is transcorneal electrical stimulation (TES). Rather than replacing pharmacological, genetic or surgical strategies, TES is being investigated as a form of neuromodulation that may support the survival and function of remaining retinal cells. Okuvision, a German medtech company, has already taken the technology into regulated clinical use in RP through its OkuStim system, and is now investigating whether the same therapeutic principle might be applicable to other degenerative eye diseases.
From experimental concept to clinical use
“In simple terms, OkuStim is an innovative, clinically tested treatment designed to slow the progression of vision loss in the degenerative retinal disease retinitis pigmentosa,” says Dr. Alfred Stett, CEO of Okuvision.
The therapy is delivered using a portable device and a fine filament electrode positioned at the lower eyelid so that it touches the surface of the eye. A weak electrical current passes through the cornea to stimulate the retina.
“The aim is to activate the retina’s own protective mechanisms, helping the remaining intact retinal cells to remain functional and survive for longer,” Stett explains.
The appeal of the concept lies partly in its independence from the mutation causing the disease. RP is genetically heterogeneous, with hundreds of causative mutations, while gene therapies are generally mutation-specific. TES, by contrast, delivers a physical stimulus and does not alter the cells genetic information. In principle, this means the approach could sit alongside other therapeutic strategies rather than precluding them.
That complementary role could be important. The future treatment landscape for degenerative eye disease is unlikely to be defined by a single modality. Gene therapy, cell-based approaches, drugs, surgery and device-based interventions may ultimately address different stages or mechanisms of disease. Electrical stimulation therefore raises a broader question: could neuromodulation become another layer in a more diversified strategy for preserving visual function?
For Okuvision, the clinical focus remains on RP. OkuStim 2 (the next generation iteration of the OkuStim device) received CE marking in 2025 and is designed for once-weekly home use after clinical adjustment and patient training. Treatment typically takes around 30 minutes. According to Stett, around 200 patients are now using the current device, either in standard RP treatment or in clinical studies in RP and glaucoma.
The evidence question
But the evidence base requires careful interpretation.
“That’s an important distinction,” says Stett. “The clinical efficacy and safety data were generated with the predecessor system, rather than with the current OkuStim 2 device.”
The CE marking of the newer device was based on a documented equivalence assessment under the European Medical Devices Regulation. The relevant technical, biological and clinical characteristics were compared, with the conclusion that previous evidence could be transferred to the updated system.
“The key point is that the dosage and delivery of the current through the filament electrode – and therefore the stimulation of the retina – have not changed,” says Stett. “On that basis, the clinical evidence collected since 2011 with the predecessor system applies to OkuStim 2.”
That evidence provides a substantial body of safety experience, but questions remain around the magnitude and durability of clinical benefit. Across clinical studies, more than 600 patients have used OkuStim, amounting to several hundred patient-years of experience. According to Stett, no serious side effects have been observed; the most common side effect is a temporary feeling of dry eyes after treatment, which can generally be prevented or relieved with lubricating eye drops.
The more difficult question is efficacy over the long course of RP. Earlier studies were limited by relatively small patient groups and follow-up periods that generally did not extend beyond 12 months. For a slowly progressive disease, that can make it difficult to establish whether an apparent slowing of visual-field loss represents a clinically meaningful and sustained effect.
“The earlier studies had two main limitations: the duration of follow-up and the size of the patient groups,” says Stett. “Because RP progresses very slowly, one year is simply too short to determine whether any slowing of visual-field loss is sustained.”
That gap is the focus of the TES-RP study, a manufacturer-independent study commissioned by Germany’s Joint Federal Committee. It followed 140 patients at 17 German eye clinics for three years and has now been completed, with publication of the results expected in 2027.
For the field, those data could prove important. “That longer follow-up and larger sample should provide a very robust answer as to whether TES can slow visual-field loss in RP over several years and whether the effect is sustained,” Stett says. “If the answer is yes, the way is clear for reimbursement in Germany.”
The importance of the study also extends beyond one device. Evidence generation in rare, slowly progressive retinal diseases is intrinsically difficult: progression can vary between patients, endpoints may be complex, and clinically meaningful change may only become apparent over long time horizons. A credible future for TES will therefore depend less on enthusiasm for the mechanism than on whether carefully designed studies can demonstrate durable patient benefit.
Beyond retinitis pigmentosa
That same discipline will be essential as Okuvision explores indications beyond RP, particularly geographic atrophy and glaucoma.
These diseases are biologically and clinically distinct, but they converge on a common problem: the progressive loss of retinal cells. In RP and geographic atrophy, photoreceptors are lost; in glaucoma, retinal ganglion cells and the optic nerve are affected.
“The rationale is biological,” Stett explains. “The neuroprotective mechanism we are targeting is not specific to a single disease; it involves more general regulatory and protective mechanisms in the eye.”
Electrical stimulation has been associated with several potentially protective processes, including anti-apoptotic mechanisms, neurotrophic signalling, effects on blood flow and anti-inflammatory mechanisms. None of that establishes clinical efficacy in a new indication, but it does provide a hypothesis worth testing.
The distinction between biological rationale and clinical proof is critical. Geographic atrophy and glaucoma both carry substantial unmet need, but the pathway from mechanistic plausibility to meaningful patient benefit is long. New indications will require disease-specific endpoints, appropriate patient selection and enough follow-up to determine whether preserved structure or function translates into outcomes that matter to patients.
In this sense, indication expansion is as much a test of the therapeutic principle as it is a development strategy. If electrical stimulation is exerting a more general neuroprotective effect, its potential relevance may extend beyond photoreceptor degeneration. But each disease will need to answer that question on its own terms.
Finding a place in the treatment landscape
That is why the next phase of TES may be less about rapid expansion than about defining where electrical stimulation truly belongs. The technology has already crossed one important threshold: it is no longer simply an experimental idea, and in RP it has been translated into a regulated, patient-oriented medical technology. The next threshold is harder. It is to establish, indication by indication, whether neuromodulation can make a reproducible and clinically meaningful difference.
For Stett, there is a clear scientific rationale for asking those questions beyond RP. “Extending the technology is not a shot in the dark; it is a logical clinical application of what cell biology tells us about retinal protection.”
If that rationale is borne out clinically, the role of electrical stimulation may ultimately be complementary rather than competitive. TES does not need to displace gene therapy, pharmacology or surgery to become relevant. It may instead find a place as one component of a broader treatment landscape focused on preserving remaining function, potentially extending therapeutic opportunities, or addressing patients for whom other approaches are unavailable.
That possibility also changes the way the technology should be judged. Rather than asking whether electrical stimulation can become a universal answer to retinal degeneration, the more useful question may be where, when and in which patients it adds meaningful value alongside other treatments.
For Okuvision, RP provides the clinical starting point. The TES-RP study will add a much-needed longer-term test of efficacy, while work in other degenerative diseases will determine whether the underlying neuroprotective rationale can travel beyond photoreceptor degeneration.
That is the real next chapter for transcorneal electrical stimulation: not simply a new device or a wider list of indications, but a test of whether controlled electrical stimulation can earn a durable place in the ophthalmic treatment landscape.
