Alogliptin-Pioglitazone (alogliptin benzoate/pioglitazone HCl)

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Last reviewed · Source: First Databank (FDB) drug data

Overview

Alogliptin benzoate, a dipeptidyl peptidase-4 (DPP-4) inhibitor, is an antidiabetic agent.

Pioglitazone, a thiazolidinedione (glitazone), is an antidiabetic agent.

Alogliptin inhibits dipeptidyl peptidase-4 (DPP-4), an enzyme that inactivates the incretin hormones: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Alogliptin selectively inhibits DPP-4 with no effect on DPP-8 or DPP-9 in vitro at concentrations approximating those from therapeutic exposures. Alogliptin increases circulating concentrations of GLP-1 and GIP in a glucose-dependent manner.

GLP-1 and GIP stimulate insulin secretion from pancreatic beta-cells in a glucose-dependent manner (i.e., when glucose concentrations are elevated). GLP-1 also decreases glucagon secretion from pancreatic alpha-cells, leading to reduced hepatic glucose production.

Alogliptin did not increase the QT interval corrected for rate (QTc) at daily dosages of 50 or 400 mg daily for 7 days in a randomized, placebo-controlled, active-comparator (moxifloxacin) study; the 400-mg dose produced plasma concentrations 19-fold higher than the maximum recommended clinical dose of 25 mg.

Following oral administration of a single dose of alogliptin (up to 800 mg) in healthy individuals, median time to peak plasma concentration was 1-2 hours; the drug has an absolute oral bioavailability of approximately 100%. Peak inhibition of DPP-4 occurs within 1--2 hours of administration with single and repeated dosing in patients with type 2 diabetes mellitus. Administration of alogliptin with food did not substantially alter total and peak exposure to the drug.

Alogliptin does not undergo extensive metabolism; 60-80% of the dose is excreted unchanged. Following administration of a radiolabeled dose of alogliptin, approximately 89% of administered radioactivity was excreted in urine (76%) and feces (13%). Terminal elimination half-life of alogliptin is approximately 21 hours following a single dose of 25 mg.

Age (range: 18--80 years), gender, and race do not have any clinically meaningful effect on the pharmacokinetics of alogliptin. Total and peak exposure to alogliptin are approximately 10% and 8% lower, respectively, in patients with moderate hepatic impairment (Child-Pugh class B); the effects of severe hepatic impairment (Child-Pugh class C) have not been studied. Exposure (as determined by plasma AUC) is increased 1.2-fold in patients with mild renal impairment (creatinine clearance >=60 to 90 mL/minute), 2-fold in patients with moderate renal impairment (creatinine clearance >=30 to <60 mL/minute), 3-fold in patients with severe renal impairment (creatinine clearance >=15 to <30 mL/minute), and 4-fold in patients with end-stage renal disease (creatinine clearance <15 mL/minute or requiring dialysis).

Pioglitazone is a thiazolidinedione (glitazone) antidiabetic agent that is structurally and pharmacologically related to troglitazone and rosiglitazone but unrelated to other antidiabetic agents, including sulfonylureas, biguanides, and alpha-glucosidase inhibitors.

Pioglitazone acts principally by increasing insulin sensitivity in target tissues, as well as decreasing hepatic gluconeogenesis. Pioglitazone is a peroxisome proliferator-activated receptorgamma (PPARgamma) agonist that increases transcription of insulin-responsive genes and increases insulin sensitivity. Pioglitazone ameliorates insulin resistance associated with type 2 diabetes mellitus without stimulating insulin release from pancreatic beta cells, thus avoiding the risk of hypoglycemia.

Because pioglitazone does not lower glucose concentrations below euglycemia, the drug is appropriately referred to as an antidiabetic agent rather than a hypoglycemic agent. Some evidence suggests that the glucoregulatory effects of thiazolidinediones are mediated in part via enhanced hepatic and peripheral glucose uptake and reduced systemic and tissue lipid availability.

Following oral administration of pioglitazone, peak plasma concentrations are achieved within 2 hours. Food delays time to peak concentrations to 3-4 hours but does not alter AUC. Pioglitazone is extensively (>99%) protein bound, principally to serum albumin.

Pioglitazone is extensively metabolized via hydroxylation and oxidation, principally via the cytochrome P-450 (CYP) 2C8 and CYP3A4 isoenzymes, with involvement of several other isoforms, including CYP1A1 (mainly an extrahepatic isoenzyme). The major circulating active metabolites of pioglitazone are M-III (keto derivative) and M-IV (hydroxyl derivative). Following oral administration, approximately 15% to 30% of the pioglitazone dose is recovered in the urine.

Renal elimination is negligible, and the drug is excreted primarily as metabolites and their conjugates. It is presumed that most of the oral dose is excreted into the bile either unchanged or as metabolites and is eliminated in the feces. The mean serum half-life of pioglitazone and its metabolites (M-III and M-IV) range from 3 to 7 hours and 16 to 24 hours, respectively.

The serum elimination half-life of pioglitazone and metabolites remains unchanged in patients with moderate (creatinine clearance 30--50 mL/minute) and severe (creatinine clearance <30 mL/minute) renal impairment when compared to subjects with normal renal function. Compared with healthy controls, subjects with impaired hepatic function (Child-Pugh class B and C) have an approximate 45% reduction in pioglitazone and total pioglitazone (pioglitazone, M-III, M-IV) mean peak plasma concentration but no change in the mean AUC values. In healthy elderly subjects, mean peak plasma concentration was not significantly different, but AUC values were approximately 21% higher than those achieved in younger subjects; the mean half-life was also prolonged (10 hours) compared to younger subjects (7 hours).

These changes observed in elderly subjects is not considered clinically relevant. The mean peak plasma concentration and AUC values of pioglitazone were increased 20% to 60% in women compared to men.

Bioequivalence has been demonstrated between the fixed combination of pioglitazone and immediate-release metformin hydrochloride and each agent given concurrently as separate tablets at the currently approved dosage strengths (500 or 850 mg of metformin hydrochloride and 15 mg of pioglitazone). Bioequivalence also has been demonstrated between the fixed combination of pioglitazone and glimepiride and each agent given concurrently as separate tablets at the currently approved dosage strengths (2 or 4 mg of glimepiride and 30 mg of pioglitazone).

USES: This combination medication is used with a proper diet and exercise program to control high blood sugar in people with type 2 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.

This product contains 2 medications: alogliptin and pioglitazone. Alogliptin works by increasing levels of natural substances called incretins. Incretins help to control blood sugar by increasing insulin release, especially after a meal.

They also decrease the amount of sugar your liver makes. Pioglitazone works by helping to restore your body's proper response to insulin.

Generic name: alogliptin benzoate/pioglitazone HCl
Pronunciation: (AL-oh-GLIP-tin/PYE-oh-GLI-ta-zone)

Reference product & biosimilars

No reference, biosimilar or interchangeable associated with this drug.

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Indications

The following indications are listed for Alogliptin-Pioglitazone:

  • Type 2 Diabetes Mellitus

Also known as: Adult Onset Diabetes, Adult Onset Diabetes Mellitus, Adult Onset Dm, Diabetes Mellitus Type 2, Diabetes Mellitus Type Ii, Ketosis-Resistant Diabetes Mellitus, Ketosis-Resistant Dm, Maturity Onset Diabetes, Maturity Onset Diabetes Mellitus, Non-Insulin Dependent Diabetes Mellitus, Non-Insulin-Dependent Diabetes Mellitus, Type Ii Diabetes Mellitus.

Dosing

Dosage of alogliptin benzoate is expressed in terms of alogliptin.

Dosage of pioglitazone hydrochloride is expressed in terms of pioglitazone.

Drug interactions

Alogliptin is principally renally excreted; cytochrome P-450 (CYP)-related metabolism is negligible.

Pioglitazone is metabolized principally by cytochrome P-450 (CYP) 2C8, and to a lesser degree, by CYP3A4, with additional contributions from a variety of isoforms including the mainly extrahepatic CYP1A1.

Pioglitazone is a weak inducer of CYP3A4.

Contraindications

*Known serious hypersensitivity (e.g., anaphylaxis, angioedema, severe cutaneous adverse reactions) to alogliptin.

*Initiation in patients with established New York Heart Association (NYHA) class III or IV heart failure (HF).

*Known serious hypersensitivity reaction to pioglitazone or any ingredient in the formulation.

Adverse reactions

Most common adverse reactions (incidence >=4%) in patients receiving alogliptin monotherapy include nasopharyngitis, headache, and upper respiratory tract infection.

Most common adverse reactions (incidence >=4%) in patients receiving alogliptin in combination with metformin include upper respiratory tract infection, nasopharyngitis, diarrhea, hypertension, headache, back pain, and urinary tract infection.

Most common adverse reactions (incidence >=4%) in patients receiving alogliptin in combination with pioglitazone include nasopharyngitis, back pain, and upper respiratory tract infection.

The most common adverse effects of pioglitazone (>=5% of patients) reported in clinical trials were upper respiratory tract infection, headache, sinusitis, myalgia, and pharyngitis.

Precautions

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ICD codes

No ICD codes are available for this drug.

Formulary status

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Last reviewed · Source: First Databank (FDB) drug data