Traditional methods of evaluating ocular pharmacokinetics are invasive and costly. Sacrificing animals at multiple time points followed by eye enucleation and isolation of different ocular tissues makes the process tedious and time consuming. Further, changes in drug location and concentration can occur during tissue extraction. In comparison, ocular fluorophotometry is a non-invasive technique, which does not affect ocular tissues and allows time course evaluations in the same animal in different ocular tissues using a single scan. In this study, we determined the delivery and pharmacokinetics of NaF injected in suprachorodial space of rats and compared it with intravitreal and posterior subconjunctival injections using ocular fluorophotometry. NaF is a rational choice for in vivo fluorophotometry because of its safety, high absorptivity, and fluorescence yield. Further, the molecular weight of NaF is similar to many antimicrobial agents and steroids administered to the eye for the treatment of ocular disorders. This is the first study to demonstrate suprachoroidal injection in a rat model and compare the pharmacokinetics of suprachoroidal injection with intravitreal and posterior subconjunctival injections using noninvasive ocular fluorophotometry. We demonstrated that 1) sodium fluorescein levels can be monitored noninvasively in different ocular tissues after suprachoroidal, posterior subconjunctival, and intravitreal injections in rats using ocular fluorophotometry; 2) the suprachoroidal route is the most effective method for attaining high concentrations of sodium fluorescein in the choroid-retina region; and 3) the rate and extent of delivery to the choroid-retina is highest with suprachoroidal injection. Baseline Fluorotron scans showed very minimal autofluorescence peaks in the choroid-retina, lens, and cornea regions. A very low autofluorescence was also observed in the anterior chamber. Autofluoresence in the choroid-retina region of rats is attributed to the presence of lipofuscin granules in the retinal pigment epithelial cells and elastin layer in the bruch’s membrane. Autofluoresence in the lens can be due to the presence of flavoproteins such as FMN in the lens epithelium. Rat corneal autofluorescence is caused by pyridine nucleotides such as nicotinamide adenine dinucleotide phosphate and flavin nucleotides such as flavin mononucleotide in metabolically active cells such as the corneal epithelium and endothelium. Baseline autofluorescence and peak assignments are shown in Figure 2A. Using fluorophotometry, we compared NaF levels in the eye after suprachoroidal, subconjunctival, and intravitreal injections. The signals observed were much higher than the background fluorescence and each route resulted in peak signals at a Niltubacin citations distinct location, corresponding to the site of injection. Suprachoroidal injection of NaF in the rat eye showed a broad peak possibly due to the ‘halation’ of the choroid-retina response. Halation or secondary fluorescence occurs due to the presence of a highly autofluorescent tissue such as choroid near the point of quantification. Light passing straight through the choroid- retina is reflected back by the choroid base and scattered around. This causes the fluorescence to bleed through and results in tailing of the choroid-retina response. Despite significant advances in understanding the mechanisms underlying this disease, current treatments for HF have not been satisfied. It is recognized that sympathetic nervous system is one of the most important mechanisms regulating cardiac function, mainly through activation of b-AR. Catecholamine such as epinephrine and norepinephrine are agonists of adrenoceptor in vivo.