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Information on the dosage, side effects, and precautions of GLUCOPHAGE and GLUCOPHAGE XR for adults and pediatric patients with type 2 diabetes. It includes details on starting doses, dose increments, maximum doses, food effects, and adverse reactions.
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HIGHLIGHTS OF PRESCRIBING INFORMATION These highlights do not include all the information needed to use GLUCOPHAGE and GLUCOPHAGE XR safely and effectively. See full prescribing information for GLUCOPHAGE and GLUCOPHAGE XR.
GLUCOPHAGE ^ (metformin hydrochloride) tablets, for oral use GLUCOPHAGE ^ XR (metformin hydrochloride) extended-release tablets, for oral use Initial U.S. Approval: 1995 WARNING: LACTIC ACIDOSIS See full prescribing information for complete boxed warning.
Renal Impairment:
FULL PRESCRIBING INFORMATION: CONTENTS WARNING: LACTIC ACIDOSIS 1 INDICATIONS AND USAGE 2 DOSAGE AND ADMINISTRATION* 2.1 Adult Dosage 2.2 Pediatric Dosage for GLUCOPHAGE 2.3 Recommendations for Use in Renal Impairment 2.4 Discontinuation for Iodinated Contrast Imaging Procedures 3 DOSAGE FORMS AND STRENGTHS 4 CONTRAINDICATIONS 5 WARNINGS AND PRECAUTIONS 5.1 Lactic Acidosis 5.2 Vitamin B 12 Deficiency 5.3 Hypoglycemia with Concomitant Use with Insulin and Insulin Secretagogues 5.4 Macrovascular Outcomes
6 ADVERSE REACTIONS 6.1 Clinical Studies Experience 6.2 Postmarketing Experience 7 DRUG INTERACTIONS 8 USE IN SPECIFIC POPULATIONS 8.1 Pregnancy 8.2 Lactation 8.3 Females and Males of Reproductive Potential 8.4 Pediatric Use 8.5 Geriatric Use 8.6 Renal Impairment 8.7 Hepatic Impairment 10 OVERDOSAGE 11 DESCRIPTION 12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action 1
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12.3 Pharmacokinetics NONCLINICAL TOXICOLOGY 13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility CLINICAL STUDIES
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16.1 How Supplied 16.2 Storage PATIENT COUNSELING INFORMATION
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14.1 GLUCOPHAGE 14.2 GLUCOPHAGE XR HOW SUPPLIED/STORAGE AND HANDLING
*Sections or subsections omitted from the full prescribing information are not listed.
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GLUCOPHAGE XR
2.2 Pediatric Dosage for GLUCOPHAGE
2.3 Recommendations for Use in Renal Impairment
2.4 Discontinuation for Iodinated Contrast Imaging Procedures
Discontinue GLUCOPHAGE/GLUCOPHAGE XR at the time of, or prior to, an iodinated contrast imaging procedure in patients with an eGFR between 30 and 60 mL/min/1.73 m^2 ; in patients with
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a history of liver disease, alcoholism, or heart failure; or in patients who will be administered intra- arterial iodinated contrast. Re-evaluate eGFR 48 hours after the imaging procedure; restart GLUCOPHAGE/GLUCOPHAGE XR if renal function is stable.
3 DOSAGE FORMS AND STRENGTHS
GLUCOPHAGE is available as:
GLUCOPHAGE XR is available as:
4 CONTRAINDICATIONS
GLUCOPHAGE and GLUCOPHAGE XR are contraindicated in patients with:
(5.1) ].
5 WARNINGS AND PRECAUTIONS
5.1 Lactic Acidosis
There have been postmarketing cases of metformin-associated lactic acidosis, including fatal cases. These cases had a subtle onset and were accompanied by nonspecific symptoms such as malaise, myalgias, abdominal pain, respiratory distress, or increased somnolence; however, hypotension and resistant bradyarrhythmias have occurred with severe acidosis. Metformin associated lactic acidosis was characterized by elevated blood lactate concentrations (>5 mmol/L), anion gap acidosis (without evidence of ketonuria or ketonemia), and an increased lactate: pyruvate ratio; metformin plasma levels were generally >5 mcg/mL. Metformin decreases liver
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cardiac impairment than younger patients. Assess renal function more frequently in elderly patients.
5.2 Vitamin B 12 Deficiency
In GLUCOPHAGE clinical trials of 29-week duration, a decrease to subnormal levels of
previously normal serum vitamin B 12 levels was observed in approximately 7% of patients. Such
decrease, possibly due to interference with B 12 absorption from the B12-intrinsic factor complex, may be associated with anemia but appears to be rapidly reversible with discontinuation of
GLUCOPHAGE or vitamin B 12 supplementation. Certain individuals (those with inadequate
vitamin B 12 or calcium intake or absorption) appear to be predisposed to developing subnormal
vitamin B 12 levels. Measure hematologic parameters on an annual basis and vitamin B 12 at 2 to 3 year intervals in patients on GLUCOPHAGE/GLUCOPHAGE XR and manage any abnormalities [see Adverse Reactions (6.1) ].
5.3 Hypoglycemia with Concomitant Use with Insulin and Insulin Secretagogues
Insulin and insulin secretagogues (e.g., sulfonylurea) are known to cause hypoglycemia. GLUCOPHAGE/GLUCOPHAGE XR may increase the risk of hypoglycemia when combined
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with insulin and/or an insulin secretagogue. Therefore, a lower dose of insulin or insulin secretagogue may be required to minimize the risk of hypoglycemia when used in combination with GLUCOPHAGE/GLUCOPHAGE XR [see Drug Interactions (7)].
5.4 Macrovascular Outcomes
There have been no clinical studies establishing conclusive evidence of macrovascular risk reduction with GLUCOPHAGE/GLUCOPHAGE XR.
6 ADVERSE REACTIONS
The following adverse reactions are also discussed elsewhere in the labeling:
6.1 Clinical Studies Experience
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
GLUCOPHAGE
In a U.S. clinical trial of GLUCOPHAGE in patients with type 2 diabetes mellitus, a total of 141 patients received GLUCOPHAGE up to 2550 mg per day. Adverse reactions reported in greater than 5% of GLUCOPHAGE treated patients and that were more common than in placebo-treated patients, are listed in Table 1.
Table 1: Adverse Reactions from a Clinical Trial of GLUCOPHAGE Occurring >5% and More Common than Placebo in Patients with Type 2 Diabetes Mellitus
GLUCOPHAGE (n=141)
Placebo (n=145) Diarrhea 53 % 12% Nausea/Vomiting 26% 8% Flatulence 12% 6% Asthenia 9% 6% Indigestion 7% 4% Abdominal Discomfort 6% 5% Headache 6% 5%
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Table 3 presents clinically significant drug interactions with GLUCOPHAGE/GLUCOPHAGE XR.
Table 3: Clinically Significant Drug Interactions with GLUCOPHAGE/GLUCOPHAGE XR
Carbonic Anhydrase Inhibitors
Clinical Impact:
Carbonic anhydrase inhibitors frequently cause a decrease in serum bicarbonate and induce non-anion gap, hyperchloremic metabolic acidosis. Concomitant use of these drugs with GLUCOPHAGE/GLUCOPHAGE XR may increase the risk for lactic acidosis. Intervention: Consider more frequent monitoring of these patients. Examples: Topiramate, zonisamide, acetazolamide or dichlorphenamide. Drugs that Reduce GLUCOPHAGE/GLUCOPHAGE XR Clearance
Clinical Impact:
Concomitant use of drugs that interfere with common renal tubular transport systems involved in the renal elimination of metformin (e.g., organic cationic transporter-2 [OCT2] / multidrug and toxin extrusion [MATE] inhibitors) could increase systemic exposure to metformin and may increase the risk for lactic acidosis [see Clinical Pharmacology (12.3)]. Intervention: Consider the benefits and risks of concomitant use with GLUCOPHAGE/GLUCOPHAGE XR. Examples: Ranolazine, vandetanib, dolutegravir, and cimetidine. Alcohol Clinical Impact: Alcohol is known to potentiate the effect of metformin on lactate metabolism. Intervention: Warn patients against excessive alcohol intake while receiving GLUCOPHAGE/GLUCOPHAGE XR. Insulin Secretagogues or Insulin
Clinical Impact:
Coadministration of GLUCOPHAGE/GLUCOPHAGE XR with an insulin secretagogue (e.g., sulfonylurea) or insulin may increase the risk of hypoglycemia. Intervention: Patients receiving an insulin secretagogue or insulin may require lower doses the insulin secretagogue or insulin.^ of Drugs Affecting Glycemic Control Clinical Impact: Certain drugs tend to produce hyperglycemia and may lead to loss of glycemic control.
Intervention:
When such drugs are administered to a patient receiving GLUCOPHAGE/GLUCOPHAGE XR, observe the patient closely for loss of blood glucose control. When such drugs are withdrawn from a patient receiving GLUCOPHAGE/GLUCOPHAGE XR, observe the patient closely for hypoglycemia.
Examples:
Thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers, and isoniazid.
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8.1 Pregnancy
Risk Summary
Limited data with GLUCOPHAGE/GLUCOPHAGE XR in pregnant women are not sufficient to determine a drug-associated risk for major birth defects or miscarriage. Published studies with metformin use during pregnancy have not reported a clear association with metformin and major birth defect or miscarriage risk [see Data]. There are risks to the mother and fetus associated with poorly controlled diabetes mellitus in pregnancy [see Clinical Considerations].
No adverse developmental effects were observed when metformin was administered to pregnant Sprague Dawley rats and rabbits during the period of organogenesis at doses up to 2- and 5 times, respectively, a 2550 mg clinical dose, based on body surface area [see Data].
The estimated background risk of major birth defects is 6–10% in women with pre-gestational diabetes mellitus with an HbA1C >7 and has been reported to be as high as 20–25% in women with a HbA1C >10. The estimated background risk of miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2–4% and 15–20%, respectively.
Clinical Considerations
Disease-associated maternal and/or embryo/fetal risk
Poorly-controlled diabetes mellitus in pregnancy increases the maternal risk for diabetic ketoacidosis, pre-eclampsia, spontaneous abortions, preterm delivery, stillbirth and delivery complications. Poorly controlled diabetes mellitus increases the fetal risk for major birth defects, stillbirth, and macrosomia related morbidity.
Data
Human Data
Published data from post-marketing studies have not reported a clear association with metformin and major birth defects, miscarriage, or adverse maternal or fetal outcomes when metformin was used during pregnancy. However, these studies cannot definitely establish the absence of any metformin-associated risk because of methodological limitations, including small sample size and inconsistent comparator groups.
Animal Data
Metformin hydrochloride did not adversely affect development outcomes when administered to pregnant rats and rabbits at doses up to 600 mg/kg/day. This represents an exposure of about 2 and 5 times a 2550 mg clinical dose based on body surface area comparisons for rats and rabbits, respectively. Determination of fetal concentrations demonstrated a partial placental barrier to metformin.
8.2 Lactation
Risk Summary
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8.6 Renal Impairment
Metformin is substantially excreted by the kidney, and the risk of metformin accumulation and lactic acidosis increases with the degree of renal impairment. GLUCOPHAGE/GLUCOPHAGE XR is contraindicated in severe renal impairment, patients with an estimated glomerular filtration rate (eGFR) below 30 mL/min/1.73 m^2 [see Dosage and Administration (2.3), Contraindications (4), Warnings and Precautions (5.1), and Clinical Pharmacology (12.3) ].
8.7 Hepatic Impairment
Use of metformin in patients with hepatic impairment has been associated with some cases of lactic acidosis. GLUCOPHAGE/GLUCOPHAGE XR is not recommended in patients with hepatic impairment. [see Warnings and Precautions (5.1) ].
10 OVERDOSAGE
Overdose of metformin hydrochloride has occurred, including ingestion of amounts greater than 50 grams. Hypoglycemia was reported in approximately 10% of cases, but no causal association with metformin has been established. Lactic acidosis has been reported in approximately 32% of metformin overdose cases [see Warnings and Precautions (5.1) ]. Metformin is dialyzable with a clearance of up to 170 mL/min under good hemodynamic conditions. Therefore, hemodialysis may be useful for removal of accumulated drug from patients in whom metformin overdosage is suspected.
11 DESCRIPTION
GLUCOPHAGE/GLUCOPHAGE XR contain the antihyperglycemic agent metformin, which is a biguanide, in the form of monohydrochloride. The chemical name of metformin hydrochloride is N,N -dimethylimidodicarbonimidic diamide hydrochloride. The structural formula is as shown below:
Metformin hydrochloride is a white to off-white crystalline compound with a molecular formula
of C 4 H11N 5 • HCl and a molecular weight of 165.63. It is freely soluble in water and is practically
insoluble in acetone, ether, and chloroform. The pKa of metformin is 12.4. The pH of a 1% aqueous solution of metformin hydrochloride is 6.68.
GLUCOPHAGE tablets contain 500 mg, 850 mg, or 1000 mg of metformin hydrochloride, which is equivalent to 389.93 mg, 662.88 mg, 779.86 mg metformin base, respectively. Each tablet contains the inactive ingredients povidone and magnesium stearate. In addition, the coating for the
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500 mg and 850 mg tablets contains hypromellose and the coating for the 1000 mg tablet contains hypromellose and polyethylene glycol.
GLUCOPHAGE XR contains 500 mg or 750 mg of metformin hydrochloride, which is equivalent to 389.93 mg, 584.90 mg metformin base, respectively.
GLUCOPHAGE XR 500 mg tablets contain the inactive ingredients hypromellose, microcrystalline cellulose, sodium carboxymethyl cellulose, and magnesium stearate.
GLUCOPHAGE XR 750 mg tablets contain the inactive ingredients hypromellose, sodium carboxymethyl cellulose, magnesium stearate and iron oxide pigment red.
12 CLINICAL PHARMACOLOGY
12.1 Mechanism of Action
Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes mellitus, lowering both basal and postprandial plasma glucose. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. With metformin therapy, insulin secretion remains unchanged while fasting insulin levels and day-long plasma insulin response may decrease.
12.3 Pharmacokinetics
Absorption
The absolute bioavailability of a GLUCOPHAGE 500 mg tablet given under fasting conditions is approximately 50% to 60%. Studies using single oral doses of GLUCOPHAGE 500 to 1500 mg and 850 to 2550 mg, indicate that there is a lack of dose proportionality with increasing doses, which is due to decreased absorption rather than an alteration in elimination. At usual clinical doses and dosing schedules of GLUCOPHAGE, steady state plasma concentrations of metformin are reached within 24 to 48 hours and are generally <1 μg/mL.
Following a single oral dose of GLUCOPHAGE XR, Cmax is achieved with a median value of 7 hours and a range of 4 to 8 hours. Peak plasma levels are approximately 20% lower compared to the same dose of GLUCOPHAGE, however, the extent of absorption (as measured by AUC) is comparable to GLUCOPHAGE.
At steady state, the AUC and Cmax are less than dose proportional for GLUCOPHAGE XR within the range of 500 to 2000 mg administered once daily. Peak plasma levels are approximately 0.6, 1.1, 1.4 and 1.8 mcg/mL for 500, 1000, 1500, and 2000 mg once-daily doses, respectively. The extent of metformin absorption (as measured by AUC) from GLUCOPHAGE XR at a 2000 mg once-daily dose is similar to the same total daily dose administered as GLUCOPHAGE tablets 1000 mg twice daily. After repeated administration of GLUCOPHAGE XR, metformin did not accumulate in plasma.
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Geriatrics
Limited data from controlled pharmacokinetic studies of GLUCOPHAGE in healthy elderly subjects suggest that total plasma clearance of metformin is decreased, the half-life is prolonged,
and Cmax is increased, compared to healthy young subjects. It appears that the change in metformin pharmacokinetics with aging is primarily accounted for by a change in renal function (see Table 4). [See Warnings and Precautions (5.1) and Use in Specific Populations (8.5) ].
Table 4: Select Mean (±S.D.) Metformin Pharmacokinetic Parameters Following Single or Multiple Oral Doses of GLUCOPHAGE
Subject Groups: GLUCOPHAGE dosea (number of subjects)
C (^) max b (mcg/mL)
Tmax c (hrs)
Renal Clearance (mL/min) Healthy, nondiabetic adults: 500 mg single dose (24) 850 mg single dose (74)d 850 mg three times daily for 19 dosese^ (9)
1.03 (±0.33) 1.60 (±0.38) 2.01 (±0.42)
2.75 (±0.81) 2.64 (±0.82) 1.79 (±0.94)
600 (±132) 552 (±139) 642 (±173) Adults with type 2 diabetes mellitus: 850 mg single dose (23) 850 mg three times daily for 19 dosese^ (9)
1.48 (±0.5) 1.90 (±0.62)
3.32 (±1.08) 2.01 (±1.22)
491 (±138) 550 (±160) Elderly f, healthy nondiabetic adults: 850 mg single dose (12) 2.45 (±0.70) 2.71 (±1.05) 412 (±98) Renal-impaired adults: 850 mg single dose Mild (CLcrg^61 - 90 mL/min) (5) Moderate (CLcr 31 - 60 mL/min) (4) Severe (CLcr 10 - 30 mL/min) (6)
1.86 (±0.52)
4.12 (±1.83) 3.93 (±0.92)
3.20 (±0.45)
3.75 (±0.50) 4.01 (±1.10)
384 (±122)
108 (±57) 130 (±90) a (^) All doses given fasting except the first 18 doses of the multiple dose studies b (^) Peak plasma concentration c (^) Time to peak plasma concentration d (^) Combined results (average means) of five studies: mean age 32 years (range 23-59 years) e (^) Kinetic study done following dose 19, given fasting f (^) Elderly subjects, mean age 71 years (range 65-81 years) g (^) CLcr = creatinine clearance normalized to body surface area of 1.73 m 2
Pediatrics
After administration of a single oral GLUCOPHAGE 500 mg tablet with food, geometric mean
metformin Cmax and AUC differed less than 5% between pediatric type 2 diabetic patients (12- years of age) and gender- and weight-matched healthy adults (20-45 years of age), all with normal renal function.
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Gender
Metformin pharmacokinetic parameters did not differ significantly between normal subjects and patients with type 2 diabetes mellitus when analyzed according to gender (males=19, females=16).
Race
No studies of metformin pharmacokinetic parameters according to race have been performed.
Drug Interactions
In Vivo Assessment of Drug Interactions
Table 5: Effect of Coadministered Drug on Plasma Metformin Systemic Exposure Coadministered Drug
Dose of Coadministered Drug *
Dose of Metformin *
Geometric Mean Ratio (ratio with/without coadministered drug) No Effect = 1. AUC †^ C^ max No dosing adjustments required for the following: Glyburide 5 mg 850 mg metformin (^) 0.91‡^ 0.93‡ Furosemide 40 mg 850 mg metformin (^) 1.09‡^ 1.22‡ Nifedipine 10 mg 850 mg metformin 1.16 1. Propranolol 40 mg 850 mg metformin 0.90 0. Ibuprofen 400 mg 850 mg metformin (^) 1.05‡^ 1.07‡ Cationic drugs eliminated by renal tubular secretion may reduce metformin elimination [See Warnings and Precautions (5.9) and Drug Interactions (7.2). ] Cimetidine 400 mg 850 mg metformin 1.40 1. Carbonic anhydrase inhibitors may cause metabolic acidosis [See Warnings and Precautions (5.1) and Drug Interactions (7.1). ] Topiramate (^) 100 mg §^ 500 mg §^ metformin (^) 1.25§^ 1.
§ (^) At steady state with topiramate 100 mg every 12 hours and metformin 500 mg every 12 hours; AUC = AUC0-12h
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Adult Clinical Studies
A double-blind, placebo-controlled, multicenter US clinical trial involving obese patients with type 2 diabetes mellitus whose hyperglycemia was not adequately controlled with dietary management alone (baseline fasting plasma glucose [FPG] of approximately 240 mg/dL) was conducted. Patients were treated with GLUCOPHAGE (up to 2550 mg/day) or placebo for 29 weeks. The results are presented in Table 7.
Table 7: Mean Change in Fasting Plasma Glucose and HbA1c at Week 29 Comparing GLUCOPHAGE vs Placebo in Patients with Type 2 Diabetes Mellitus
GLUCOPHAGE (n=141)
Placebo (n=145)
p-Value
FPG (mg/dL) Baseline Change at FINAL VISIT
–53.
NS*
Hemoglobin A (^) 1c (%) Baseline Change at FINAL VISIT
–1.
NS*
Mean baseline body weight was 201 lbs and 206 lbs in the GLUCOPHAGE and placebo arms, respectively. Mean change in body weight from baseline to week 29 was -1.4 lbs and -2.4 lbs in the GLUCOPHAGE and placebo arms, respectively.A 29-week, double-blind, placebo-controlled study of GLUCOPHAGE and glyburide, alone and in combination, was conducted in obese patients with type 2 diabetes mellitus who had failed to achieve adequate glycemic control while on maximum doses of glyburide (baseline FPG of approximately 250 mg/dL). Patients randomized to the combination arm started therapy with GLUCOPHAGE 500 mg and glyburide 20 mg. At the end of each week of the first 4 weeks of the trial, these patients had their dosages of GLUCOPHAGE increased by 500 mg if they had failed to reach target fasting plasma glucose. After week 4, such dosage adjustments were made monthly, although no patient was allowed to exceed GLUCOPHAGE 2500 mg. Patients in the GLUCOPHAGE only arm (metformin plus placebo) discontinued glyburide and followed the same titration schedule. Patients in the glyburide arm continued the same dose of glyburide. At the end of the trial, approximately 70% of the patients in the combination group were taking GLUCOPHAGE 2000 mg/glyburide 20 mg or GLUCOPHAGE 2500 mg/glyburide 20 mg. The results are displayed in Table 8.
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Table 8: Mean Change in Fasting Plasma Glucose and HbA1c at Week 29 Comparing GLUCOPHAGE/Glyburide (Comb) vs Glyburide (Glyb) vs GLUCOPHAGE (GLU): in Patients with Type 2 Diabetes Mellitus with Inadequate Glycemic Control on Glyburide
Comb (n=213)
Glyb (n= )
GLU (n=210)
p-Values Glyb vs Comb GLU vs Comb GLU vs Glyb
Fasting Plasma Glucose (mg/dL) Baseline 250.5 247.5 253.9 NS* NS* NS* Change at FINAL VISIT – 63.5 13.7 – 0.9 0.001 0.001 0. Hemoglobin A (^) 1c (%) Baseline 8.8 8.5 8.9 NS* NS* 0. Change at FINAL VISIT – 1.7 0.2 – 0.4 0.001 0.001 0.
Mean baseline body weight was 202 lbs, 203 lbs, and 204 lbs in the GLUCOPHAGE/glyburide, glyburide, and GLUCOPHAGE arms, respectively. Mean change in body weight from baseline to week 29 was 0.9 lbs, -0.7 lbs, and -8.4 lbs in the GLUCOPHAGE/glyburide, glyburide, and GLUCOPHAGE arms, respectively.
Pediatric Clinical Studies
A double-blind, placebo-controlled study in pediatric patients aged 10 to 16 years with type 2 diabetes mellitus (mean FPG 182.2 mg/dL), treatment with GLUCOPHAGE (up to 2000 mg/day) for up to 16 weeks (mean duration of treatment 11 weeks) was conducted. The results are displayed in Table 9.
Table 9: Mean Change in Fasting Plasma Glucose at Week 16 Comparing GLUCOPHAGE vs Placebo in Pediatric Patientsa^ with Type 2 Diabetes Mellitus
GLUCOPHAGE Placebo p-Value FPG (mg/dL) Baseline Change at FINAL VISIT
(n=37)
(n=36)
21.4 <0. a (^) Pediatric patients mean age 13.8 years (range 10- 16 years)
Mean baseline body weight was 205 lbs and 189 lbs in the GLUCOPHAGE and placebo arms, respectively. Mean change in body weight from baseline to week 16 was -3.3 lbs and -2.0 lbs in the GLUCOPHAGE and placebo arms, respectively.
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