Myopia, or nearsightedness, has quickly become a global public health challenge. Once considered a largely benign condition, it is now recognised as a major risk factor for irreversible visual impairment later in life. The World Health Organization (WHO) estimates that, if current trends continue, half of the world’s population could be myopic by 2050, with roughly 10 percent developing high myopia. This severe form of the condition thins and weakens the retina and optic nerve, increasing the risk of retinal detachment, glaucoma, and myopic macular degeneration.
The rise in myopia prevalence is being driven in part by lifestyle changes, particularly among children. Increased time spent indoors, prolonged screen times, and reduced exposure to natural daylight have all been implicated. As a result, epidemiological data suggest that global myopia prevalence has tripled since 1990, rising to 36 percent globally.
Crucially, myopia often begins early in childhood — typically between six and seven years of age — and progresses through adolescence. The earlier onset occurs, the higher the likelihood that a child will develop high myopia. This has sharpened the focus on interventions that can slow or halt excessive axial elongation of the eye.
A new candidate, 7-methylxanthine (7-MX), has attracted interest as the first myopia control pharmaceutical for oral use. 7-MX has been shown to reduce experimental myopia in preclinical models, while clinical data suggest it may slow myopia progression in children and adolescents.
Limits of existing interventions
A key point about myopia is that it’s cumulative over many years. “Take a child who develops myopia at seven. Over the next six years, the excess, unnecessary elongation of the eye will be around 1.4 millimeters,” Klaus Trier, ophthalmologist and cofounder of Theialife, told DDN. “So whatever treatment you are proposing, that’s the benchmark it has to be measured against.”
Today’s myopia-control strategies fall into two main categories: optical and pharmacological. Optical approaches focus on slowing axial elongation in children by correcting vision while simultaneously altering peripheral or central retinal defocus. Short-term randomized trials have shown that certain lens designs can significantly reduce axial length growth, with estimated (extrapolated) reductions of 0.4–0.75mm over six years. However, their efficacy often declines over time and rebound effects are well documented once treatment stops.
Pharmacological intervention has been dominated by atropine eye drops. To achieve a robust effect, several studies have shown that a concentration of 0.05 percent is most effective. In randomized trials, this dose has been associated with reductions in axial elongation of around 0.05–0.06mm in the first year of treatment. While statistically significant, this translates to approximately 0.15–0.18mm over six years — only a small fraction of the 1.4mm benchmark. Moreover, atropine is associated with dose-dependent side effects, including light sensitivity and blurred near vision, and discontinuation is frequently followed by rebound acceleration of myopia progression. Due to this, a concentration of 0.01 percent is most commonly prescribed, which achieves a modest slowing of axial elongation — typically on the order of 0.1–0.2mm reduction over a few years compared with controls.
Revisiting an old drug
7-MX is a caffeine metabolite that has been investigated for myopia control for more than two decades. Preclinical studies across multiple animal models — including guinea pigs, rabbits, and rhesus monkeys — have shown that 7-MX inhibits excessive axial elongation in both form-deprivation and lens-induced myopia. And, in Denmark, oral 7-MX has been used under compassionate-use and investigator-initiated protocols since 2009, with more than 1,200 children receiving the compound.
A large Danish cohort study of more than 700 children, followed for an average of 3.6 years between 2000 and 2021, showed a clear dose-dependent association between 7-MX exposure and reduced myopia progression. For a typical child starting treatment at age seven, nine, or eleven and taking an average dose of 1,000mg per day, the model predicted 0.07mm less axial elongation after one year, 0.16mm after three years, and 0.18mm after six years. While these annual differences are modest, they accumulate over time — consistent with the slow, progressive nature of myopia. And most importantly, eye growth appears to return to age-expected rates after discontinuation, without evidence of rebound acceleration.
“With 7-MX, we don’t see the same gradual decline in efficacy over time [as existing treatments],” said Trier. “We have follow-up data out to five years and beyond, and the effect appears to be sustained. And we don’t see a rebound effect when treatment stops.”
Additionally, no side effects have been reported to the Danish Medicines Agency since the drug was approved for use in 2009, including in children who have taken 7-MX continuously for 10 years. This is likely because the drug has poor ability to penetrate the blood-brain barrier, limiting its effects to peripheral tissues and reducing the risk of central nervous system side effects.
A different biological target
The difference in rebound effect likely comes down to mechanism. “Both atropine and optical devices seem to work, at least in part, by thickening a layer of the eye called the choroid. That thickening is reversible, so when treatment stops, the choroid thins again — and that’s likely one reason you see rebound progression,” explained Trier.
7-MX, in contrast, has been shown in animal studies to increase collagen content, widen collagen fibrils, and thicken the posterior sclera. More recent work suggests that this effect is mediated through inhibition of the A2A adenosine receptor (ADORA2A). Adenosine is a metabolic by-product that accumulates during periods of high retinal activity, such as in low-light conditions.
“When you close your eyes, the retina actually works harder, which leads to an increase in adenosine,” explained Trier. “That’s interesting because many theories about the myopia epidemic point to reduced exposure to sunlight. If children spend more time indoors and get less daylight, the retina remains in a state of chronically high metabolism, adenosine accumulates, and in that sense, it may not be unreasonable to block that receptor.”
Another key aspect is dopamine. “Dopamine has long been linked to myopia, but in the opposite direction — low dopamine levels are associated with myopia development. Dopamine is stimulated by light exposure, so adenosine and dopamine are essentially oppositely regulated.”
Trier explained that the receptors for these two neurotransmitters are also physically linked, meaning that when you activate one receptor, you suppress the other. “So, if you block the adenosine receptor, you effectively enhance dopamine signaling.”
From immediate release to ND10
One limitation of early 7-MX studies has been pharmacokinetics. The compound has a short half-life, producing a rapid serum spike followed by swift elimination, which limits its effect. In previous studies, this has meant taking as many as three tablets a day.
Theialife has now developed ND10, a sustained-release formulation of 7-MX. By maintaining more stable systemic exposure, ND10 is designed to enhance efficacy without increasing dose burden. Theialife is now preparing to initiate Phase 3 clinical trials, where, if successful, ND10 could represent a first-in-class oral therapy for pediatric myopia.
As childhood myopia continues its global rise, the development of mechanistically distinct therapies is essential. Whether ND10 ultimately fulfils that promise will depend on forthcoming Phase 3 data — but the concept of an oral, non-rebounding intervention is already reshaping expectations of what myopia control might look like in the years ahead.
