Tight control of presumed critical risk factors now is apparently inadequate in reducing the occurrence of picture threatening proliferative retinopathy. Furthermore Fingolimod cost towards the established risk factors, evidence is suggested by genomic linkage analysis for a genetic predisposition to produce diabetic retinopathy. It’s obvious that discovery treatment options and targeted treatment methods are expected to produce inroads into the treatment of this devastating condition that threatens a growing amount of diabetics. 2. Recent Pharmacological Options to Combat Angiogenesis in Diabetic Retinopathy Anti VEGF A therapeutics has changed into a dominant strategy for the management of ocular neovascular diseases. Ongoing clinical trials for diabetic retinopathy mainly concentrate on a mechanism of actionmediated via VEGF An antagonism. Of the 103 currently available NIH sponsored clinical trials concerning Immune system diabetic retinopathy, the majorities are directed at therapy of diabetic macular edema and proliferative diabetic retinopathy using Lucentis, Avastin, and to a lesser degree Macugen either as single agents, in combination with other pharmacological agents, or in combination with laser photocoagulation therapy. Within the past eight years, two drugs targeting VEGF were approved for fighting ocular neo-vascularization. Both these Macugen, drugs and Lucentis were approved for exudative age relatedmacular deterioration. Now, Lucentis has received approval for use in patients suffering visual impairment because of macular edema secondary to central and branch retinal vein occlusion. The anti HDAC1 inhibitor VEGF monoclonal antibody drug Avastin happens to be used off-label for wet macular degeneration. The success of anti-vegf remedies has created an unprecedented understanding of the factors and pathogenic mechanisms operant in several retinal neovascular conditions and has demonstrated that therapeutic agents considered initially only in the realm of anticancer agents have demonstrated efficacy in combating ocular neovascularization. May the same story be coming for mTOR inhibitors for which the key indication in addition has been in the treatment of cancers? Other antiangiogenic approaches for ocular angiogenic conditions contain progress elements, steroid compounds, or kinase inhibitors. No mTOR inhibitors which target the mammalian target of rapamycin are currently being clinically evaluated due to their efficacy in nonproliferative or proliferative stages of diabetic retinopathy. Only two mTOR substances, Sirolimus and Palomid 529 are currently being evaluated in NIH sponsored trials for ocular indications. Sirolimus is being evaluated to take care of diabetic macular edema which really is a frequent manifestation of diabetic retinopathy, for ARMD, and for uveitis. Palomid 529 will be evaluated for ARMD.