Awiqli Flextouch (insulin icodec-abae)
Intermediate-, Long-acting, and Combination Insulins Subcutaneous Insulin Pen (ML)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Insulin icodec-abae is a long-acting human insulin analog prepared using recombinant DNA technology.
Insulin icodec-abae is a long-acting human insulin analog prepared using recombinant DNA technology and chemically modified to include a C20 fatty acid side chain that binds to albumin. The drug lowers blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, inhibiting hepatic glucose production, inhibiting lipolysis and proteolysis, and enhancing protein synthesis. Insulin icodec-abae has an extended half-life due to its ability to bind reversibly to albumin, creating a depot in the circulation from which the drug is slowly released.
The insulin receptor is activated by insulin icodec leading to a stable glucose-lowering effect over 1 week.
Steady-state concentrations of insulin icodec-abae are achieved within 2-4 weeks. The peak glycemic response and nadir are observed on day 2 and day 7, respectively, following an injection. Plasma protein binding of insulin icodec-abae is >99%.
The half-life of insulin icodec is approximately 1 week. Age, sex, race, ethnicity, and hepatic/renal impairment do not appear to meaningfully affect drug exposure.
USES: Insulin icodec is used with a proper diet and exercise program to control high blood sugar in people with diabetes. Controlling high blood sugar helps prevent kidney damage, blindness, nerve problems, loss of limbs, and sexual function problems. Proper control of diabetes may also lessen your risk of a heart attack or stroke.
Insulin icodec is a man-made product that is similar to human insulin. It replaces the insulin that your body would normally make. It acts longer than regular insulin, providing a low, steady level of insulin.
It works by helping blood sugar (glucose) get into cells so your body can use it for energy. Insulin icodec may be used with a shorter-acting insulin product. It may also be used alone or with other diabetes drugs.
Generic name: insulin icodec-abae
Drug class: Intermediate-, Long-acting, and Combination Insulins
Therapeutic class: Endocrine
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
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Indications
No indications are available for this drug.
Dosing
The insulin icodec-abae FlexTouch pen delivers doses in 10-unit increments up to 700 units in a single injection.
The dosage of insulin should be individualized and titrated based on the patient's metabolic needs, blood glucose monitoring results, and glycemic control goals. Dose modifications may be needed with changes in renal or hepatic function or during illness. Due to the long half-life of insulin icodec-abae, dose adjustment is not advised during acute illness or short-term changes in physical activity level or diet. Consider other appropriate interventions, such as adjustments to glucose intake or concomitant glucose-lowering medications.
No dosing information is available for this tab.
| Drug label | Dosing type | Instructions |
|---|---|---|
| Awiqli Flextouch 700 Unit/Ml | Maintenance | Inject by subcutaneous route per prescriber's instructions. Insulin dosing requires individualization. |
No dosing information is available for this tab.
Drug interactions
There is no enhanced messaging for this drug.
Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
Agents Affecting Growth Hormone/Macimorelin
SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
MECHANISM OF ACTION: Agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test.(1)
CLINICAL EFFECTS: Concurrent use of agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of macimorelin states concurrent use with agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test. Discontinue growth hormone products at least 1 week before administering the macimorelin diagnostic test. Sufficient washout time of drugs affecting growth hormone release prior to administration of macimorelin is recommended.(1) Agents affecting growth hormone include: - Drugs that directly affect the pituitary secretion of growth hormone (e.g. somatostatin, insulin, glucocorticoids, cyclooxygenase inhibitors) - Drugs that may transiently elevate growth hormone concentrations (e.g. clonidine, levodopa, insulin) - Drugs that may blunt the growth hormone response (e.g. muscarinic antagonists, anti-thyroid medications, growth hormone products)
DISCUSSION: Concurrent use of agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test.(1)
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Antidiabetic Agents/Gatifloxacin
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The exact mechanism is unknown.
CLINICAL EFFECTS: Concurrent use of gatifloxacin may result in hypoglycemia and/or hyperglycemia.(1-4) Hypoglycemia is more common during the first three days of concurrent therapy. Hyperglycemia is more common after the first three days of concurrent therapy.(2)
PREDISPOSING FACTORS: Elderly patients, especially those with decreased renal function may be predisposed to this interaction.(2)
PATIENT MANAGEMENT: Patients receiving concurrent gatifloxacin should be closely monitored for hypoglycemia during the first three days of concurrent therapy and for hyperglycemia after the first three days of concurrent therapy. Patients should be instructed to discontinue gatifloxacin if hypoglycemia or hyperglycemia occur.(2)
DISCUSSION: Hypoglycemia has been reported with gatifloxacin and glyburide(1,5,6) or glimepiride.(7) In a study in patients with type 2 diabetes mellitus, concurrent gatifloxacin (400 mg daily for 10 days) had no effect on the pharmacokinetics of glyburide (steady state daily regimen); however, pharmacodynamic interactions have been reported.(2) Health Canada has received 19 reports of hypoglycemia in patients taking gatifloxacin. Seventeen of these involved concurrent hypoglycemic agents. Health Canada has received 2 reports of hyperglycemia in patients taking gatifloxacin and hypoglycemic agents. Health Canada has received 2 reports of patients experiencing hypoglycemia and hyperglycemia during concurrent gatifloxacin and hypoglycemic agents.(3) In a study, 13 reports of dysglycemia were reported in patients taking gatifloxacin. Ten of these patients had diabetes mellitus and were on concurrent hypoglycemic agents. Of these ten patients, nine patients experienced hypoglycemia, while one patient experienced hyperglycemia.(8)
Insulin/Rosiglitazone
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The exact mechanism is unknown, but may be the result of additive fluid retention.(1,2)
CLINICAL EFFECTS: The concurrent use of rosiglitazone and insulin may increase the risk of edema, heart failure, and other cardiovascular effects such as myocardial infarction.(1,2)
PREDISPOSING FACTORS: Use in patients with NYHA Class I and II heart failure may increase the risk of other cardiovascular events.(1,2)
PATIENT MANAGEMENT: The US manufacturer of rosiglitazone states that concurrent use with insulin is not recommended.(1) If concurrent therapy is warranted, patients should be monitored for cardiovascular adverse events. If signs and symptoms of congestive heart failure develop, patients should be treated according to current standards of care. Consideration should be given to lowering the dosage of or discontinuing rosiglitazone.(2)
DISCUSSION: In a meta-analysis of 7 controlled, randomized, double-blind clinical trials in which patients were randomized to coadministration of rosiglitazone with insulin or insulin alone, the incidence of congestive heart failure in patients receiving concurrent rosiglitazone was 2.3%, compared with 1.0% in patients receiving insulin alone. More patients in the concurrent rosiglitazone group experienced myocardial infarctions, MACE (a composite of myocardial infarction, cardiovascular death, or stroke), cardiovascular deaths, and all-cause deaths than in the group receiving insulin alone.(1) In clinical trials, edema was reported in 14.7% of patients receiving concurrent rosiglitazone and insulin, compared with 5.4% on insulin alone or 4.8% on rosiglitazone alone.(1) In clinical trials, new onset or exacerbation of congestive heart failure occurred at rates of 1%, 2%, and 3%, respectively, in patients treated with insulin alone, insulin with 4 mg of rosiglitazone, and insulin with 8 mg of rosiglitazone.(1)
Moderate Interaction: Assess the risk to the patient and take action as needed.
Antidiabetic Agents/Gymnema
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Gymnema has been shown to increase the number of insulin-secreting beta cells in animals. It has also been shown to increase the activity of enzymes responsible for glucose uptake and utilization and inhibit peripheral utilization of glucose.(1)
CLINICAL EFFECTS: Use of gymnema may result in decreased requirements of antidiabetic agents.(2-4)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Diabetic patients should be carefully monitored if gymnema is initiated or discontinued from concurrent therapy. The dosage of the patient's antidiabetic agent(s) may need to be adjusted.(2)
DISCUSSION: In a study in 22 non-insulin-dependent patients, patients had decreased blood glucose, glycosylated hemoglobin, and glycosylated plasma proteins during gymnema therapy. Patients were able to decrease the dosage of their conventional antidiabetic therapy and five patients were able to discontinue their conventional antidiabetic therapy.(3) In a study in 27 insulin-dependent patients, patients had decreased insulin requirements, fasting blood glucose, glycosylated hemoglobin, and glycosylated plasma protein levels.(4)
Antidiabetics/Epinephrine
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Gluconeogenesis, glycogenolysis, and lipolysis are increased by epinephrine. Also, insulin secretion and glucose uptake by peripheral tissues are decreased by epinephrine.
CLINICAL EFFECTS: Increased blood glucose resulting in decreased effectiveness of the antidiabetic agent.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Caution when starting or stopping epinephrine in diabetic patients. Adjust the antidiabetic dose as needed based on blood glucose levels.
DISCUSSION: This interaction is likely to occur based upon well documented properties of the interacting drugs. However, there is individual variability in its occurrence.
Antidiabetics/Slt Ophth Non-Cardioselective Beta-Blockers
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Not fully established. Probably blockade of a variety of beta-adrenergic responses to hypoglycemia.(1,2)
CLINICAL EFFECTS: Diminished response to sulfonylureas and insulin may occur. Frequency and severity of hypoglycemic episodes may be increased, while warning symptoms of low blood sugar may be masked.(1,2)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Try to avoid beta-blocker therapy, particularly in diabetics prone to hypoglycemic attacks. One of the cardioselective agents may decrease risk of hypertensive attacks and allow more rapid glucose recovery from hypoglycemia. Patients should be counseled not to rely on tachycardia to diagnose hypoglycemia, since it is masked by beta-blocker therapy. Diaphoresis is unaffected by beta-blockade and can be used by the diabetic to recognize hypoglycemia.
DISCUSSION: A double blind, randomized, 12 month study of 39 patients tested the metabolic effects of pindolol (5mg BID) compared to control group on insulin sensitivity. The patient's insulin sensitivity index decreased 17% when on pindolol treatment compared to placebo (p<0.01). Insulin mediated glucose uptake was significantly lower (p<0.05) with propranolol treatment than with placebo.(3) A study of 26 patients with chronic heart failure showed that carvedilol (average daily dose 27.5mg/d) caused a significant decrease in fasting insulin levels (17.09 to 10.77 microU/ml, p <0.05) compared to pre-treatment levels. This trial also showed that patients on carvedilol had significantly (p=0.015) lower fasting insulin levels (10.77 microU/ml) compared to the fasting insulin levels (20.72 microU/ml) of patients on bisoprolol treatment (5.9mg/d).(4) There have been case reports of hypoglycemia following the addition of ophthalmic timolol to a diabetic regimen.(5-7) Studies have shown that ophthalmic beta-blockers, especially the aqueous solution, have significant systemic absorption and do not undergo first-pass metabolism.(8,9)
Hypoglycemics; Insulin/Bupropion
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Bupropion can lower the seizure threshold and when given concurrently with other medications that also lower the threshold there is an increased risk of seizure. Concurrent use of hypoglycemics or insulin increases the risk of hypoglycemia which can result in seizures.(1,2)
CLINICAL EFFECTS: Concurrent use of bupropion and hypoglycemics or insulin may increase the risk of seizure.(1,2)
PREDISPOSING FACTORS: The risk of seizures may be increased in patients with a history of head trauma or prior seizure; CNS tumor; severe hepatic cirrhosis; excessive use of alcohol or sedatives; addiction to opiates, cocaine, or stimulants; use of over-the-counter stimulants an anorectics; a total daily dose of bupropion greater than 450 mg or single doses greater than 150 mg; rapid escalation of bupropion dosage; or with concomitant medications known to lower seizure threshold (antidepressants, antipsychotics, systemic steroids, theophylline).(1,2)
PATIENT MANAGEMENT: The use of bupropion in patients treated with oral hypoglycemic agents or insulin should be undertaken only with extreme caution and with low initial bupropion dosing and small gradual dosage increases.(1,2) Single doses should not exceed 150 mg.(1,2) The maximum daily dose of bupropion should not exceed 300 mg for smoking cessation(2) or 450 mg for depression.(1)
DISCUSSION: Because of the risk of seizure from concurrent bupropion and other agents that lower seizure threshold, the manufacturer of bupropion states that the concurrent use of bupropion and oral hypoglycemic agents or insulin should be undertaken only with extreme caution and with low initial bupropion dosing and small gradual dosage increases.(1,2)
Insulin/Carvedilol; Labetalol
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Not fully established. Probably blockade of a variety of beta-adrenergic responses to hypoglycemia.
CLINICAL EFFECTS: Diminished response to insulin may occur. Frequency and severity of hypoglycemic episodes may be increased, while warning symptoms of low blood sugar may be masked.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Try to avoid beta-blocker therapy, particularly in diabetics prone to hypoglycemic attacks. One of the cardioselective agents may decrease risk of hypertensive attacks and allow more rapid glucose recovery from hypoglycemia. Patients should be counseled not to rely on tachycardia to diagnose hypoglycemia, since it is masked by beta-blocker therapy. Diaphoresis is unaffected by beta-blockade and can be used by the diabetic to recognize hypoglycemia.
DISCUSSION: A class effect of diminished glucose-lowering effects is expected with concurrent use of beta-blockers and insulin. It is prudent to monitor serum glucose closely in patients receiving beta-blocker therapy because symptoms of hypoglycemia may be masked. A double blind, randomized, 12 month study of 39 patients tested the metabolic effects of pindolol (5 mg BID) compared to control group on insulin sensitivity. The patient's insulin sensitivity index decreased 17% when on pindolol treatment compared to placebo (p<0.01). Insulin mediated glucose uptake was significantly lower (p<0.05) with propranolol treatment than with placebo. (1) A study of 26 patients with chronic heart failure showed that carvedilol (average daily dose 27.5 mg/d) caused a significant decrease in fasting insulin levels (17.09 to 10.77 microU/ml, p <0.05) compared to pre-treatment levels. This trial also showed that patients on carvedilol had significantly (p=0.015) lower fasting insulin levels (10.77 microU/ml) compared to the fasting insulin levels (20.72 microU/ml) of patients on bisoprolol treatment (5.9mg/d).(2)
Insulin/Fenfluramine;Dexfenfluramine
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Fenfluramine increases glucose uptake at the receptor site (ie, skeletal muscle).
CLINICAL EFFECTS: The hypoglycemic effect of insulin is increased.
PREDISPOSING FACTORS: Diabetes.
PATIENT MANAGEMENT: In diabetic patients receiving insulin, monitor blood glucose levels and observe the patient for signs of hypoglycemia when initiating therapy with fenfluramine and for symptoms of hyperglycemia when fenfluramine is discontinued.
DISCUSSION: When administered before meals or to fasting patients, fenfluramine has been found to have hypoglycemic action. Numerous reports have demonstrated fenfluramine to potentiate the hypoglycemic effect of insulin in diabetic patients.
Insulin/Pioglitazone
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The exact mechanism is unknown, but may be the result of additive fluid retention.(1,2)
CLINICAL EFFECTS: The concurrent use of pioglitazone with insulin may increase the risk of edema and heart failure.(1,2)
PREDISPOSING FACTORS: Specific risk factors for heart failure could not be determined. Patients with ongoing edema are more likely to have edema-associated adverse effects with combination therapy.(1)
PATIENT MANAGEMENT: Patients receiving concurrent therapy should be monitored for cardiovascular adverse events. If signs and symptoms of congestive heart failure develop, patients should be treated according to current standards of care. Consideration should be given to lowering the dosage of or discontinuing pioglitazone.(1,2)
DISCUSSION: In a clinical trial, two of 191 (1.1%) of patients receiving pioglitazone (15 mg) and insulin and two of 188 (1.1%) of patients receiving pioglitazone (30 mg) and insulin developed congestive heart failure. None of the patients receiving insulin alone developed congestive heart failure.(1)
Insulin/Selected Systemic Non-Cardioselective Beta-Blockers
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Not fully established. Probably blockade of a variety of beta-adrenergic responses to hypoglycemia. MECHANISM OF ACTION: Not fully established. Probably blockade of a variety of beta-adrenergic responses to hypoglycemia.
CLINICAL EFFECTS: Diminished response to insulin may occur. Frequency and severity of hypoglycemic episodes may be increased, while warning symptoms of low blood sugar may be masked. CLINICAL EFFECTS: Diminished response to insulin may occur. Frequency and severity of hypoglycemic episodes may be increased, while warning symptoms of low blood sugar may be masked.
PREDISPOSING FACTORS: None determined. PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Try to avoid beta-blocker therapy, particularly in diabetics prone to hypoglycemic attacks. One of the cardioselective agents may decrease risk of hypertensive attacks and allow more rapid glucose recovery from hypoglycemia. Patients should be counseled not to rely on tachycardia to diagnose hypoglycemia, since it is masked by beta-blocker therapy. Diaphoresis is unaffected by beta-blockade and can be used by the diabetic to recognize hypoglycemia. PATIENT MANAGEMENT: Try to avoid beta-blocker therapy, particularly in diabetics prone to hypoglycemic attacks. One of the cardioselective agents may decrease risk of hypertensive attacks and allow more rapid glucose recovery from hypoglycemia. Patients should be counseled not to rely on tachycardia to diagnose hypoglycemia, since it is masked by beta-blocker therapy. Diaphoresis is unaffected by beta-blockade and can be used by the diabetic to recognize hypoglycemia.
DISCUSSION: A class effect of diminished glucose-lowering effects is expected with concurrent use of beta-blockers and insulin. It is prudent to monitor serum glucose closely in patients receiving beta-blocker therapy because symptoms of hypoglycemia may be masked. A double blind, randomized, 12 month study of 39 patients tested the metabolic effects of pindolol (5 mg BID) compared to control group on insulin sensitivity. The patient's insulin sensitivity index decreased 17% when on pindolol treatment compared to placebo (p<0.01). Insulin mediated glucose uptake was significantly lower (p<0.05) with propranolol treatment than with placebo. (1) A study of 26 patients with chronic heart failure showed that carvedilol (average daily dose 27.5 mg/d) caused a significant decrease in fasting insulin levels (17.09 to 10.77 microU/ml, p <0.05) compared to pre-treatment levels. This trial also showed that patients on carvedilol had significantly (p=0.015) lower fasting insulin levels (10.77 microU/ml) compared to the fasting insulin levels (20.72 microU/ml) of patients on bisoprolol treatment (5.9mg/d).(2) DISCUSSION: A class effect of diminished glucose-lowering effects is expected with concurrent use of beta-blockers and insulin. It is prudent to monitor serum glucose closely in patients receiving beta-blocker therapy because symptoms of hypoglycemia may be masked. A double blind, randomized, 12 month study of 39 patients tested the metabolic effects of pindolol (5 mg BID) compared to control group on insulin sensitivity. The patient's insulin sensitivity index decreased 17% when on pindolol treatment compared to placebo (p<0.01). Insulin mediated glucose uptake was significantly lower (p<0.05) with propranolol treatment than with placebo. (1) A study of 26 patients with chronic heart failure showed that carvedilol (average daily dose 27.5 mg/d) caused a significant decrease in fasting insulin levels (17.09 to 10.77 microU/ml, p <0.05) compared to pre-treatment levels. This trial also showed that patients on carvedilol had significantly (p=0.015) lower fasting insulin levels (10.77 microU/ml) compared to the fasting insulin levels (20.72 microU/ml) of patients on bisoprolol treatment (5.9mg/d).(2)
Selected Antidiabetic Agents/Chloroquine; Hydroxychloroquine
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The exact mechanism is unknown. Chloroquine and hydroxychloroquine may increase insulin sensitivity by inhibiting insulin metabolism and inflammation and increasing cellular uptake of glucose and glycogen synthesis.(1,2) These effects may result in additive hypoglycemia with anti-diabetic agents.
CLINICAL EFFECTS: Concurrent use of chloroquine or hydroxychloroquine and antidiabetic agents may result in severe hypoglycemia.(3) Hypoglycemia can lead to coma.
PREDISPOSING FACTORS: Elderly patients, especially those with decreased renal function may be predisposed to this interaction.
PATIENT MANAGEMENT: Patients maintained on antidiabetic agents who require concurrent therapy with chloroquine or hydroxychloroquine should be closely monitored for hypoglycemia. A decrease in the dose of insulin or other anti-diabetic medications may be required. Patients should be advised of the risk and symptoms of hypoglycemia and to contact their doctor if hypoglycemia occurs.(3) Signs of hypoglycemia may include confusion, dizziness, feeling shaky, unusual hunger, headaches, irritability, pounding heart or very fast pulse, pale skin, sweating, trembling, weakness, or unusual anxiety.
DISCUSSION: Hydroxychloroquine has been shown to cause severe hypoglycemia including loss of consciousness that could be life threatening.(3) Concomitant hypoglycemic agents may increase the risk and/or severity of this effect. A 77 year old man who was stable on twice daily insulin suffered two episodes of hypoglycemic coma 2 weeks after starting prednisone 5 mg daily and hydroxychloroquine 400 mg daily for rheumatoid arthritis. His insulin dosage required a decrease of 37%.(4) Many studies have investigated the glucose-lowering effect of hydroxychloroquine. In a clinical trial of type II diabetics on maximal doses of sulfonylureas, addition of hydroxychloroquine lowered hemoglobin A1C (HbA1C) up to 1% more than placebo.(5) Another clinical trial of type II diabetics on metformin and glimepiride or gliclazide found that hydroxychloroquine 400 mg daily reduced fasting blood glucose (FBG), post-prandial glucose (PPG), and HbA1C to a similar degree as pioglitazone 15 mg daily at 24 weeks.(6) In a prospective observational study, 250 uncontrolled type II diabetics on metformin, glimepiride, pioglitazone, sitagliptin, and a SGLT-2 inhibitor received hydroxychloroquine 400 mg daily for 48 weeks. HbA1C decreased from 8.83% to 6.44%, FBG decreased by 40.78%, and PPG decreased by 58.95%. The doses of metformin were reduced by 50%, glimepiride and sitagliptin by 75%, and SGLT-2 inhibitors were discontinued in most patients.(7)
Selected Antidiabetic Agents/Selected Quinolones
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The exact mechanism is unknown.
CLINICAL EFFECTS: Concurrent use of quinolones and antidiabetic agents may result in severe hypoglycemia.(1-7) Hypoglycemia can lead to coma.
PREDISPOSING FACTORS: Elderly patients, especially those with decreased renal function may be predisposed to this interaction.(5)
PATIENT MANAGEMENT: Patients maintained on antidiabetic agents who require concurrent therapy with a quinolone should be closely monitored for hypoglycemia.(1-4) Patients should be instructed to discontinue quinolone use and contact their doctor if hypoglycemia occurs.(2,4) Signs of hypoglycemia may include confusion, dizziness, feeling shaky, unusual hunger, headaches, irritability, pounding heart or very fast pulse, pale skin, sweating, trembling, weakness, or unusual anxiety.
DISCUSSION: Hypoglycemia has been reported with concurrent ciprofloxacin and glyburide,(1,8,9) levofloxacin and glyburide,(2,10,11) norfloxacin and glyburide,(3) levofloxacin and glipizide (12) as well as levofloxacin and metformin-glibenclamide.(14) There has been one report of fatal hypoglycemia with concurrent levofloxacin and glyburide(9) and one of the above reports of hypoglycemia with concurrent levofloxacin and glyburide resulted in hypoxic brain injury.(11) A review of postmarketing adverse event data for the fluoroquinolones and hypoglycemic coma identified 56 reports in FAERS search from October 1987- April 2017 and 11 additional cases in the medical literature. Most patients had risk factors for hypoglycemia. 41 patients were taking one or more hypoglycemic drugs. 13 deaths occurred (some of these patients had renal insufficiency). 9 patients did not fully recover and had resultant disability.(13)
Selected Antidiabetics/Maois
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The exact mechanism by which MAO inhibitors affect carbohydrate metabolism and subsequent enhancement of the hypoglycemic action of insulin is not clear. The adrenergic response to hypoglycemia may be blocked by insulin release caused by MAOI's. In vitro studies have shown that MAO inhibitors are capable of both potentiating and inhibiting insulin release, depending on their concentrations. Stimulation of glucose-mediated insulin secretion is believed to be related to the MAO inhibitory effects of the drugs.
CLINICAL EFFECTS: The hypoglycemic response to both insulin and glucose lowering agents including alpha glucosidase inhibitors, meglitinides, and sulfonylurea may be increased.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Concurrent MAO inhibitor therapy for depression in a diabetic patient will often require reduction in dosage of the hypoglycemic agent because of enhanced hypoglycemic effects. Since the extent of the reaction is highly unpredictable, any diabetic patients receiving MAO inhibitors should be monitored for possible excessive hypoglycemia.
DISCUSSION: This interaction is likely to occur. The interaction between MAOIs and insulin is well documented. Additional documentation is necessary to confirm the potential interaction of MAOI's with other glucose lowering agents including alpha glucosidase inhibitors, meglitinides, and sulfonylureas but is expected to occur based on pharmacologic similarity. It may take several weeks for the full hypoglycemic effect of the MAOI to occur. Conversely, it may take several weeks for the effect to dissipate after stopping the MAOI. Furazolidone is known to be a monoamine oxidase inhibitor. Methylene blue, when administered intravenously, has been shown to reach sufficient concentrations to be a potent inhibitor of MAO-A. Metaxalone is a weak inhibitor of MAO.
Selected Antidiabetics/Safinamide
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The exact mechanism by which MAO inhibitors such as safinamide affect carbohydrate metabolism and subsequent enhancement of the hypoglycemic action of insulin is not clear. The adrenergic response to hypoglycemia may be blocked by insulin release caused by MAOI's. In vitro studies have shown that MAO inhibitors are capable of both potentiating and inhibiting insulin release, depending on their concentrations. Stimulation of glucose-mediated insulin secretion is believed to be related to the MAO inhibitory effects of the drugs.
CLINICAL EFFECTS: The hypoglycemic response to both insulin and glucose lowering agents including alpha glucosidase inhibitors, meglitinides, and sulfonylurea may be increased.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Concurrent MAO inhibitor therapy for depression in a diabetic patient will often require reduction in dosage of the hypoglycemic agent because of enhanced hypoglycemic effects. Since the extent of the reaction is highly unpredictable, any diabetic patients receiving MAO inhibitors should be monitored for possible excessive hypoglycemia.
DISCUSSION: This interaction is likely to occur. The interaction between MAOIs and insulin is well documented. Additional documentation is necessary to confirm the potential interaction of MAOI's with other glucose lowering agents including alpha glucosidase inhibitors, meglitinides, and sulfonylureas but is expected to occur based on pharmacologic similarity. It may take several weeks for the full hypoglycemic effect of the MAOI to occur. Conversely, it may take several weeks for the effect to dissipate after stopping the MAOI.
Contraindications
*During episodes of hypoglycemia.
*Hypersensitivity to insulin icodec-abae or any of its excipients.
There are no contraindication contraindications for this drug.
- Hypoglycemic disorder
- Disease of liver
- Hypokalemia
- Kidney disease with reduction in glomerular filtration rate (GFr)
Adverse reactions
The most common adverse reactions reported in patients receiving insulin icodec-abae include hypoglycemia, hypersensitivity reactions (e.g., urticaria, swelling face and lips), injection site reactions, lipodystrophy, pruritus, rash, edema, and weight gain.
Less Frequent
- Hypersensitivity drug reaction
- Hypertension
Rare or Very Rare
- Anaphylaxis
- Angioedema
- Bronchospastic pulmonary disease
- Dyspnea
- Hypoglycemic disorder
- Hypokalemia
- Hypotension
- Localized cutaneous amyloidosis
- Tongue swelling
More Frequent
- Pharyngitis
Less Frequent
- Back pain
- Bronchitis
- Cataracts
- Cough
- Depression
- Edema
- Injection site sequelae
- Lipodystrophy
- Peripheral edema
- Rhinitis
- Sinusitis
- Skin rash
- Urinary tract infection
- Weight gain
Rare or Very Rare
- Diarrhea
- Headache disorder
- Lip swelling
- Pruritus of skin
- Subcutaneous nodules
- Upper respiratory infection
- Urticaria
Precautions
No enhanced messaging available.
Safety and efficacy of insulin icodec-abae have not been established in pediatric patients.
There are no available data regarding use of insulin icodec-abae in pregnant women to inform a drug-associated risk for major birth defects and miscarriage. Poorly controlled diabetes in pregnancy increases the maternal risk for diabetic ketoacidosis, pre-eclampsia, spontaneous abortions, preterm delivery, and delivery complications. Poorly controlled diabetes increases the fetal risk for major birth defects, still birth, and macrosomia related morbidity.
It is not known whether insulin icodec-abae is distributed into human milk, or if the drug has any effects on the breastfed infant or on milk production. Consider the developmental and health benefits of breastfeeding along with the mother's clinical need for insulin icodec-abae and any potential adverse effects on the breastfed infant from the drug or from the underlying maternal condition.
The manufacturer makes no specific dosage recommendations for geriatric patients. In older patients with diabetes mellitus, the initial dosage, dose increments, and maintenance dosage should be conservative to avoid hypoglycemia. More frequent glucose monitoring is recommended, with individualized insulin dosage adjustments as needed.
Of the 1,880 patients treated with insulin icodec-abae in clinical trials, 646 (34.4%) were >=65 years of age and 97 (5.2%) were >=75 years of age. No overall differences in safety or effectiveness have been observed between patients >=65 years of age and younger adult patients. Use caution when administering insulin icodec-abae to geriatric patients, as some older adults may be more sensitive to its effects. Hypoglycemia may be more difficult to recognize in elderly patients.
ICD codes
No ICD codes are available for this drug.
Formulary status
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Last reviewed · Source: First Databank (FDB) drug data
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