Deferoxamine Mesylate (DFOM) is an iron chelator and iron death inhibitor. Deferoxamine Mesylate binds free iron into a stable complex and reduces iron accumulation. Deferoxamine Mesylate up-regulates HIF-1α levels and induces apoptosis.

Befetupitant (Ro67-5930) is a potent and selective tachykinin 1 receptor (NK1R) antagonist for the study of corneal neovascularization.

Triciribine phosphate (VD 002) is a highly selective AKT inhibitor that induces cell cycle arrest and cysteinyl asparagin-dependent apoptosis, inhibits neovascularization, and can be used in the study of leukemia.

Burixafor hydrobromide (TG-0054 hydrobromide) is an orally bioavailable and potent CXCR4 antagonist and an anti-angiogenic drug that is of potential value in treating choroid neovascularization.

INCA-6 (Triptycene-1,4-quinone) is a cell-permeable NFAT inhibitor. INCA-6 inhibits of CN-NFAT signaling by targeting of NFAT(P) substrate to the calcineurin (CN) phosphatase site.

Arginyl-Glutamine, a dipeptide, has been shown to reduce VEGF levels and inhibit retinal neovascularization in a mouse model of oxygen-induced retinopathy [1].

(±)11(12)-EET is a fully racemic version of the R/S enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes.[1][2][3[]A higher proportion of 11(R),12(S)-EET is produced by the CYP450 isoforms CYP2C23 and CYP2C24 while CYP2B2 produces a higher proportion of 11(S),12(R)-EET.[3]11(12)-EET has been shown, along with 8(9)-EET to play a role in the recovery of depleted calcium pools in cultured smooth muscle cells[4] It also inhibits basolateral 18-pS potassium channels in the renal cortical collecting duct when used at a concentration of 100 nM.[5]11(12)-EET (50 μg/kg per day) increases adhesion of isolated peripheral blood leukocytes in a chamber coated with P-selectin and ICAM-1 but does not affect choroidal neovascularization size following laser photocoagulation[6] It also has anti-inflammatory, angiogenic, and cardioprotective properties[7]

IMS2186 is a reagent with activity of antichoroidal neovascularization (CNV). IMS2186 could arrest cancer cell cycle in G2/M phase, result in exerting anti-proliferation and anti-angiogenesis effects. IMS2186 reduces the amount of eye leakage and diseased cells with no intraocular toxicity.

Ruboxistaurin is a PKC beta inhibitor. Ruboxistaurin reduces oxidative stress and attenuates left ventricular hypertrophy and dysfunction in rats with streptozotocin-induced diabetes. Ruboxistaurin attenuates diabetic nephropathy via modulation of TGF-β1/

Ruboxistaurin mesylate monohydrate is a PKC beta inhibitor potentially for the treatment of diabetic nephropathy and diabetic macular edema. Ruboxistaurin attenuates diabetic nephropathy via modulation of TGF-β1/Smad and GRAP pathways. Ruboxistaurin reduces oxidative stress and attenuates left ventricular hypertrophy and dysfunction in rats with streptozotocin-induced diabetes. Ruboxistaurin inhibits retinal neovascularization via suppression of phosphorylation of ERK1/2 and Akt.

CGC 11093 is a polyamine analog; inhibits growth of human prostate tumor xenografts in nude mice. It may prove useful in promoting regression of choroidal neovascularization.

Tie2 Inhibitor 7 blocks Tie2 kinase activity with a Ki value of 1.3 μM.. It has been shown to inhibit angiopoietin 1-induced Tie2 autophosphorylation and downstream signaling with an IC50 value of 0.3 μM. This compound can prevent endothelial cell tube formation and aberrant vessel growth in a rat model of Matrigel-induced choroidal neovascularization.

Oltipraz (RP 35972) is a synthetic dithiolethione with potential chemopreventive and anti-angiogenic properties. Oltipraz induces phase II detoxification enzymes, such as glutathione S transferase (GST) and NAD(P)H: quinone oxidoreductase 1 (NQO1). The induction of detoxification enzymes enhances the detoxification of certain cancer-causing agents, thereby enhancing their elimination and preventing carcinogen-induced DNA damages. Although the exact mechanism through which the anti-angiogenesis effect remains to be fully elucidated, oltipraz maybe able to modulate the expression of a number of angiogenic factors, thereby blocking the sustained and focal neovascularization in multiple tumor cell types.

SF0166 is a potent, selective antagonist of α v β 3, demonstrating IC 50 values of 0.6 nM for α v β 3, 8 nM for α v β 6, and 13 nM for α v β 8. It effectively inhibits cellular adhesion to vitronectin in human, rat, rabbit, and dog cell lines, with IC 50 values ranging from 7.6 pM to 76 nM. Additionally, SF0166 significantly reduces neovascularization in the oxygen-induced retinopathy mouse model.

AGN-199659 is a novel tyrosine kinase inhibitor. It also blocks choroidal neovascularization.

MK-0626 is a Dipeptidyl peptidase IV (DPP-4) inhibitor, improving neovascularization by increasing both the number of circulating endothelial progenitor cells and endothelial nitric oxide synthetase expression.

ABT-510 is synthetic peptide that mimics the anti-angiogenic activity of the endogenous protein thrombospondin-1 (TSP-1). ABT-510 inhibits the actions of several pro-angiogenic growth factors important to tumor neovascularization; these pro-angiogenic growth factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF)), hepatocyte growth factor (HGF), and interleukin 8 (IL-8).

Bucillamine (DE019) protects against Ischemia/reperfusion injury in high-risk organ transplants and inhibits the production of VEGF. Bucillamine is an orally active sulfhydryl donor and antioxidant with antirheumatic and antiangiogenic properties. Bucillamine can be used for studies about choroidal neovascularization and rheumatoid arthritis.