2-[(1,3-ジヒドロ-3-オキソ-5-スルホ-2H-インドール)-2-イリデン]-2,3-ジヒドロ-3-オキソ-1H-インドール-5-スルホン酸

Approximately 4-9 minutes after indigotindisulfonate sodium is administered intravenously, its blue color is detectable at the ureteral orifices, enabling easier visualization for accuracy during medical procedures. Although indigotindisulfonic acid and its salt form indigotindisulfonate sodium were initially acknowledged as pharmacologically inert, their use has been associated with cardiovascular effects. Indigotindisulfonate sodium may lead to transient alpha-receptor stimulation, manifested as increased total peripheral vascular resistance, increased diastolic and systolic blood pressure, and increased central venous pressure with decreased cardiac output, stroke volume and heart rate. The use of indigotindisulfonate sodium may lead to severe or life-threatening cardiovascular reactions such as cardiac arrest, arrhythmia, asystole, second-degree atrioventricular block, hypotension, elevation in blood pressure, bradycardia, and tachycardia. Serious anaphylactic reactions with hypotension, dyspnea, bronchospasm, urticaria, or erythema have also been reported. Also, the use of indigotindisulfonate sodium may interfere with light absorption and pulse oximetric methods.

Indigotindisulfonic acid is a biologically inert blue dye. After intravenous injection, indigotindisulfonic acid is excreted by the kidney through tubular secretion and, with its deep blue color, it enhances visualization of the ureteral orifices. Because of this, indigotindisulfonic acid is used to identify ureteral patency in urologic and gynecologic procedures. Indigotindisulfonic acid may lead to the development of hypertension. It has been suggested that indigotindisulfonic acid inhibits endothelium-dependent relaxation at the level of nitric oxide generation and/or its release from the endothelium. Also, indigotindisulfonic acid appears to inhibit vascular guanylyl cyclase in smooth muscle.

Indigotindisulfonate sodium is mainly oxidized via primary metabolic pathways. An _in vivo_ study done in rats showed that the breakdown of indigotindisulfonate sodium (FD&C Blue No. 2) generated two products: isatin-5-sulphonic acid and 5-sulphoanthranilic acid. Clinical studies evaluating indigotindisulfonate sodium metabolism products have not been performed.

In healthy adults given 5 ml of indigotindisulfonate sodium (salt form of indigotindisulfonic acid), the Cmax and AUC0-INF were 6.33 μg/mL and 1.15 μg·h/mL, respectively. Studies evaluating the pharmacokinetic properties of intravenous indigotindisulfonate sodium in patients with renal impairment have not been performed. Based on subgroup analyses in a randomized clinical trial, patients with mild to moderate renal impairment or an estimated glomerular filtration rate (eGFR) from 30 to 89 mL/min do not require dose adjustments. Indigotindisulfonate sodium is not recommended in patients with eGFR lower than 30 mL/min.

Indigotindisulfonic acid is excreted largely by the kidneys, retaining its blue color during passage through the body. Approximately 16% of the unchanged drug is excreted in urine, and less than 2% is excreted in feces. The elimination of this dye begins rapidly after injection, appearing in the urine within 5 minutes.

The volume of distribution of indigotindisulfonate sodium is 10.7 L.

In healthy adults given 5 ml of indigotindisulfonate sodium, the mean urinary clearance was 7.08 L/hour, and the mean total clearance was 40.2 L/hour.