Duport

Duport is indicated as an adjunct to insulin therapy to improve glycaemic control in adults with type 1 diabetes mellitus with a Body Mass Index (BMI) ≥27 kg/m
2
, who have failed to achieve adequate glycaemic control despite optimal insulin therapy.

Sotagliflozin is administered by the oral route. The recommended dose is 200 mg sotagliflozin once daily before the first meal of the day. After at least three months, if additional glycaemic control is needed, in patients tolerating sotagliflozin 200 mg, the dose may be increased to 400 mg once daily.

Hypotension, renal impairment, hepatic impairment, genital mycotic infections, urinary tract infections, nausea, vomiting, or abdominal pain, excessive thirst, constantly feeling tired, high levels of ketones in urine tests or beta-hydroxybutyrate (BHB) in blood tests, difficulty breathing/rapid, deep breathing, difficulty paying attention, or confusion, rapid weight loss.

Hypotension
: Before initiating Duport, volume status should be assessed and correction on hypovolemia should be made in the elderly, in patients with renal impairment, in patients with low systolic blood pressure and in patients on diuretics since Duport causes intravascular volume contraction.
Impairment in Renal Function
: Renal function should be evaluated prior to initiating Duport and periodically. Initiation of Duport is not recommended when eGFR is less than 60 ml/min/1.73 m
2
and should be discontinued if eGFR is persistently less than 45 mL/min/1.73 m
2
Hepatic impairment
: Duport is not recommended in patients with moderate and severe hepatic impairment, as Duport exposure is increased in these patients.
Genital mycotic infections
: Monitoring and treatment should be done as appropriate.
Urinary tract infections
: Temporary interruption of Duport should be considered when treating pyelonephritis and urosepsis.

Sotagliflozin is an orally delivered dual inhibitor of SGLT1 and SGLT2. Sotagliflozin improves glycaemic and metabolic control through dual inhibition - local inhibition of SGLT1 in the gut and systemic SGLT2 inhibition in the proximal renal tubule. Inhibition of SGLT1 delays and reduces glucose absorption in the proximal intestine, resulting in a blunting and delay of postprandial hyperglycaemia. Inhibition of SGLT2 reduces renal glucose reabsorption and lowers the renal threshold for glucose, and thereby increases urinary glucose excretion.