KSI 201 for Wet AMD
Age-related macular degeneration (AMD) is a degenerative disease of the retina. Wet AMD is caused when blood vessels meant to nourish the retina instead are dysregulated and invade through the retina. In the short term, these neovessels are immature and leak fluid into the retina causing visual distortion and acute blindness. Over the longer term, other disease pathologies such as inflammation and fibrosis lead to photoreceptor death and atrophy.
KSI 201 is a novel, single agent, multi-inhibitor biologic in development. KSI 201 is anticipated to provide greater efficacy, more durability of efficacy, and less frequent administration.
KSI 301 for Diabetic Retinopathy
Diabetes is the leading cause of blindness among working-age adults. Diabetic retinopathy is caused by elevated blood sugar levels over time. In its early stages, blood vessels in the retina are damaged and leak fluid. In advanced stages, new and abnormal blood vessels form which may break and bleed. Fluid and hemorrhage interfere with vision and may further cause irreversible visual impairment due to retinal scarring and retinal detachment.
KSI 301 is a novel biologic in development that may block the ocular effects of high blood sugar levels, potentially preventing or slowing the progression of diabetic eye disease.
KSI 401 FOR DRY AMD
Dry AMD is a disease caused by a sustained local inflammation in the eye. Deposits of inflammatory substances accumulate on the retina. Over years and even decades, photoreceptors become damaged permanently. Biochemical, genetic, and clinical data suggest that a hyperactive complement system is a primary driver of this inflammation. The complement system is part of our innate immunity which is an evolutionarily ancient arm of our immune system. In healthy tissues, the complement system is tightly regulated. In dry AMD, the complement system is out of balance leading to disease and eventual blindness.
KSI 401 is a novel biologic in development that blocks activation of the complement system, potentially lessening disease activity in dry AMD patients.
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