Baqsimi
Baqsimi Uses, Dosage, Side Effects, Food Interaction and all others data.
Baqsimi is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia. Baqsimi raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.
Baqsimi was granted FDA approval on 14 November 1960.
Baqsimi is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia. Baqsimi raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose. Baqsimi has a short duration of action. Baqsimi may cause hyperglycemia in diabetic patients.
| Trade Name | Baqsimi |
| Availability | Prescription only |
| Generic | Glucagon |
| Glucagon Other Names | Glucagon, Glucagon (recombinant dna origin), Glucagon recombinant, Glucagon, human, Glucagon, porcine, Glucagone, Glucagonum |
| Related Drugs | mannitol, Tubersol, arginine, Baqsimi, inulin, diazoxide, Ceretec, Gvoke, GlucaGen |
| Type | |
| Formula | C165H249N49O51S1 |
| Weight | 3767.1 Da |
| Protein binding | Glucagon has not been described in the literature as bound to a protein in serum. |
| Groups | Approved |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | Canada, United States, |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Baqsimi is a form of recombinant glucagon used to treat hypoglycemia in diabetes mellitus and as a part of gastrointestinal imaging procedures.
Baqsimi is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.
Baqsimi is also used to associated treatment for these conditions: Severe Hypoglycemia
How Baqsimi works
Baqsimi binds to the glucagon receptor activating Gsα and Gq. This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A. Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium. Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.
Baqsimi also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.
Toxicity
Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.
The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.
Food Interaction
No interactions found.Baqsimi Drug Interaction
Unknown: diphenhydramine, diphenhydramine, glucose, glucose, insulin lispro, insulin lispro, insulin glargine, insulin glargine, furosemide, furosemide, insulin aspart, insulin aspart, acetaminophen, acetaminophen, cyanocobalamin, cyanocobalamin, cholecalciferol, cholecalciferol, ondansetron, ondansetron
Baqsimi Disease Interaction
Major: insulinoma, pheochromocytomaModerate: cardiac disease, glycogen depletion
Volume of Distribution
The volume of distribution of glucagon is 0.25L/kg. The apparent volume of distribution is 885L.
Elimination Route
A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes. An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.
Half Life
The half life of glucagon is 26 minutes for an intramuscular dose. The half life of glucagon nasal powder is approximately 35 minutes. The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.
Clearance
A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.
Elimination Route
Elimination of glucagon is not fully characterized in literature, however the kidney and liver appear to contribute significantly in animal models. The liver and kidney are responsible for approximately 30% of glucagon elimination each.
Innovators Monograph
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