MacuCLEAR lead proprietary compound MC1101 is being developed to treat the dry form of AMD. Challenging conventional wisdom, this novel compound is delivered in eye drop form.

While novel in this ophthalmic application, the active ingredient of MC1101 has been previously approved by the FDA as an oral antihypertensive drug. Its safety and toxicity profile is well characterized. MC1101 has been granted 505 (b) 2 status and has formal Fast Track designation by the FDA.

MacuCLEAR, Inc.’s Technology Objective is to prevent the progression of Dry AMD to Wet AMD by:

  • Restoring choroidal blood flow
  • Preventing the rupture of the Bruch’s Membrane
  • Treating aging effects of inflammation and oxidative stress

Diabetic retinopathy and other retinal diseases will also be investigated with MacuCLEAR’s portfolio of drug candidates.

Preventing the Progression of Macular Degeneration


MC-1101 treats dry AMD and prevents the progression to wet AMD based on a vascular model. Throughout the body blood brings nutrients to tissues and takes waste away. Aging can cause a reduction in blood flow as in atherosclerosis, causing two simultaneous reactions: 1) waste accumulation begins to occur. 2) new blood vessels begin to form to supplant the compromised ones. Waste accumulation can lead to a rupture of the Bruch’s Membrane, a critical blood barrier separating the retina tissues and the choroidal blood vessels. Neovascularization occurring below this membrane can then get through this opening and ultimately break down and bleed into the retinal tissues causing the wet form of AMD.

The fundamental difference between dry AMD and wet AMD is the integrity of the Bruch’s Membrane. MacuCLEAR’s mechanism of action prevents the rupture of this critical blood barrier as it:

  1. Restores choroidal blood flow
  2. Controls inflammation
  3. Restores retinal pigment epithelium (RPE) function through anti-oxidative effects

MacuCLEAR’s approach to treating Dry AMD found support in the works of several AMD researchers:

The etiology of AMD, I believe, is largely attributable to impairment of choroidal perfusion. … The model suggests that treatment of early AMD can be best accomplished by prevention or treatment of systemic atherosclerosis. … Other theories of AMD are compatible with progression and late AMD, including… oxidative damage… and inflammation.
Ephraim Friedman, MD, The Pathogenesis of Age Related Macular Degeneration; Am J Ophthalmology, 2008, Editorial
Borrowing from work in cardiovascular disease, we can convert this hypothesis into rationale for creating new model systems and new diagnostic techniques, preventions and treatments…
Christine A. Curcio, Ph.D., The Oil Spill in Bruch's Membrane; First Biennial AMD Symposium, 2010
Little is known about the structural and molecular basis of exchange between the fenestrated choriocapillaris and the RPE/photoreceptors, but it is reasonable to posit that dysfunction of this neurovacular unit contributes to age-related maculopathy.
David T. Shima, Ph.D., Probing the Molecular Basis of Vascular Barrier Function and Macromolecular Exchange at the Chorio-retina Interface; First Biennial AMD Symposium, 2010