Jolavi

Jolavi Uses, Dosage, Side Effects, Food Interaction and all others data.

An ethanolamine derivative that is an adrenergic alpha agonist. It is used as a vasoconstrictor agent in the treatment of hypotension.

Jolavi is a prodrug, i.e., the therapeutic effect of orally administered midodrine is due to the major metabolite desglymidodrine formed by deglycination of midodrine. Administration of midodrine results in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension of various etiologies. Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10-mg dose of midodrine, with some effect persisting for 2 to 3 hours. Jolavi has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.

Jolavi
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Jolavi
Availability	Prescription only
Generic	Midodrine
Midodrine Other Names	Midodrin, Midodrina, Midodrine, Midodrinum
Related Drugs	phenylephrine, norepinephrine, ephedrine, Levophed, droxidopa, ProAmatine
Weight	2.5mg
Type	Tablet
Formula	C₁₂H₁₈N₂O₄
Weight	Average: 254.2823 Monoisotopic: 254.126657074
Groups	Approved
Therapeutic Class
Manufacturer	Jolly Healthcare
Available Country	India
Last Updated:	September 19, 2023 at 7:00 am

Uses

Jolavi is an alpha-adrenergic antagonist used to treat orthostatic hypotension.

For the treatment of symptomatic orthostatic hypotension (OH).

Jolavi is also used to associated treatment for these conditions: Symptomatic Orthostatic Hypotension

How Jolavi works

Jolavi undergoes metabolism to form its pharmacologically active metabolite, desglymidodrine. Desglymidodrine acts as an agonist at the alpha₁-adrenergic receptors expressed in the arteriolar and venous vasculature. Activation of alpha₁-adrenergic receptor signaling pathways lead to an increase in the vascular tone and elevation of blood pressure. Desglymidodrine is reported to have negligible effect on the cardiac beta-adrenergic receptors.

Toxicity

Symptoms of overdose could include hypertension, piloerection (goosebumps), a sensation of coldness and urinary retention. The single doses that would be associated with symptoms of overdosage or would be potentially life- threatening are unknown. The oral LD₅₀ is approximately 30 to 50 mg/kg in rats, 675 mg/kg in mice, and 125 to 160 mg/kg in dogs. Desglymidodrine is dialyzable.

Food Interaction

Take with or without food. The absorption is unaffected by food.

Jolavi Hypertension interaction

[Major] Jolavi can cause marked elevation of supine blood pressure (BP>200 mmHg systolic) and should not be used in patients with persistent and excessive supine hypertension.

Systolic elevations of this degree are most likely to be observed in patients with relatively elevated pre-treatment systolic blood pressures (mean 170 mmHg).

There is no experience in patients with initial supine systolic pressure above 180 mmHg, as those patients were excluded from the clinical trials.

Use of midodrine in such patients is not recommended.

Additionally, care should be taken when using this agent in orthostatic hypotensive patients who are also diabetic.

Supine and sitting hypertension should be evaluated at the beginning of therapy, and blood pressure (supine, sitting, and orthostatic) should be monitored regularly.

Jolavi Disease Interaction

Major: hypertension/diabetes, hypertensive effects, renal dysfunctionModerate: hepatic dysfunction

Elimination Route

Rapidly absorbed following oral administration. The peak plasma concentrations of the prodrug, desglymidodrine, is reached about half an hour following drug administration. The metabolites reach their peak plasma concentrations at about 1 to 2 hours following drug administration. The absolute bioavailability of midodrine (measured as desglymidodrine) is 93% and is not affected by food. As desglymidodrine displays poor diffusibility across the blood-brain barrier, it is expected to have minimal effects on the central nervous system.