Objective: To assess the efficacy and safety of the glucagon-like peptide-1 receptor agonist (GLP-1 RA) efpeglenatide versus placebo in patients with type 2 diabetes inadequately controlled with diet and exercise alone. Research design and methods: AMPLITUDE-M was a phase 3, double-blind, placebo-controlled, multicenter trial that randomized adults with type 2 diabetes suboptimally controlled with diet and exercise alone to once-weekly efpeglenatide (2 mg, 4 mg or 6 mg) or placebo for up to 56 weeks. The primary objective was to demonstrate the superiority of efpeglenatide versus placebo for HbA1c reduction at week 30. Secondary objectives included changes in other measures of glycemic control and body weight at weeks 30 and 56. Results: At week 30, HbA1c was reduced from a baseline of 8.1% (65 mmol/mol) to 6.9% (52 mmol/mol), 6.6% (49 mmol/mol) and 6.4% (47 mmol/mol) with efpeglenatide 2, 4 and 6 mg, respectively. Least squares (LS) mean HbA1c reductions from baseline were statistically superior for each efpeglenatide dose versus placebo (2 mg: −0.5% [95% confidence interval [CI] −0.9,−0.2; p=0.0054]; 4 mg: −0.8% [95% CI −1.2,−0.5; p<0.0001]; 6 mg: −1.0% [95% CI −1.4,−0.7; p<0.0001]). A greater proportion of efpeglenatide-treated patients (all doses) achieved HbA1c <7% (53 mmol/mol) versus placebo by week 30 (p<0.0001 for all), and significant reductions in body weight and fasting plasma glucose were also observed for efpeglenatide (4 and 6 mg doses) versus placebo at week 30 (p<0.05 for all). Consistent with the GLP-1 RA class, gastrointestinal adverse events were most commonly reported; these were generally transient and mild/moderate in severity. Few patients reported hypoglycemia. Conclusions: As monotherapy in patients with type 2 diabetes, once-weekly efpeglenatide significantly improved glycemic control and body weight with a safety and tolerability profile similar to other GLP-1 RAs.

Efpeglenatide (Efpeg) is being developed as a long-acting GLP-1 receptor agonist for once weekly, subcutaneous administration. The efficacy and safety of Efpeg vs. placebo (PBO) was assessed in patients with type 2 diabetes (T2D) inadequately controlled with diet and exercise alone. In this double-blind, PBO-controlled, 30+26-week Phase 3 study, patients with T2D were randomized to Efpeg 2 mg (n=100), 4 mg (n=101), and 6 mg (n=103), or PBO (n=102). Endpoints were change from baseline in HbA1c at week 30 (primary) and other parameters of glycemic control, body weight (BW) and safety at weeks 30 and 56 (secondary). Baseline characteristics and key results are shown in the Table. All doses of Efpeg showed significantly greater reductions in HbA1c vs. PBO at weeks 30 and 56, and a greater proportion of patients achieved HbA1c <7%. BW was significantly reduced vs. PBO at week 30 with Efpeg 4 mg and 6 mg. Efpeg was well tolerated and the most common AEs were gastrointestinal in nature and mild to moderate in severity. Only one Efpeg-treated patient experienced a single episode of severe hypoglycemia.In conclusion, Efpeg as monotherapy in patients with T2D was well tolerated and demonstrated significant improvements versus PBO in HbA1c and BW after 30 weeks of treatment. These improvements generally remained stable through 56 weeks of therapy.View largeDownload slideView largeDownload slide DisclosureS. Baek: Employee; Self; Hanmi Pharmaceutical. J. P. Frias: Consultant; Self; 89bio, Inc., Altimmune, Axcella Health Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Gilead Sciences, Inc., Intercept Pharmaceuticals, Inc., Merck & Co., Inc., Novo Nordisk, Pfizer Inc., Sanofi, Research Support; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Bristol-Myers Squibb Company, CymaBay Therapeutics, Eli Lilly and Company, Intercept Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Madrigal Pharmaceuticals, Inc., Merck & Co., Inc., Novartis Pharmaceuticals Corporation, Novo Nordisk, Pfizer Inc., Sanofi, Speaker’s Bureau; Self; Merck & Co., Inc., Sanofi. L. Popescu: Employee; Self; Sanofi. E. Niemoeller: Employee; Self; Sanofi-Aventis Deutschland GmbH, Stock/Shareholder; Self; Sanofi. I. Muehlen-bartmer: Employee; Self; Sanofi-Aventis Deutschland GmbH. J. Rosenstock: Board Member; Self; Applied Therapeutics, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Intarcia Therapeutics, Inc., Novo Nordisk, Oramed Pharmaceuticals, Inc., Sanofi, Consultant; Self; Applied Therapeutics, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Intarcia Therapeutics, Inc., Novo Nordisk, Oramed Pharmaceuticals, Inc., Sanofi, Research Support; Self; Applied Therapeutics, AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Genentech, Inc., Intarcia Therapeutics, Inc., Lexicon Pharmaceuticals, Inc., Novartis Pharmaceuticals Corporation, Novo Nordisk, Oramed Pharmaceuticals, Inc., Pfizer Inc., REMD Biotherapeutics, Sanofi.

OBJECTIVE:Recent European Guidelines for Diabetes, Prediabetes and Cardiovascular Diseases introduced a shift in managing patients with type 2 diabetes at high risk for or established cardiovascular (CV) disease by recommending GLP-1 receptor agonists and SGLT-2 inhibitors as initial glucose-lowering therapy. This is questioned since outcome trials of these drug classes had metformin as background therapy. In this post hoc analysis, the effect of dulaglutide on CV events was investigated according to the baseline metformin therapy by means of a subgroup analysis of the Researching Cardiovascular Events with a Weekly Incretin in Diabetes (REWIND) trial. RESEARCH DESIGN AND METHODS:Patients in REWIND (n = 9901; women: 46.3%; mean age: 66.2 years) had type 2 diabetes and either a previous CV event (31%) or high CV risk (69%). They were randomized (1:1) to sc. dulaglutide (1.5 mg/weekly) or placebo in addition to standard of care. The primary outcome was the first of a composite of nonfatal myocardial infarction, nonfatal stroke, and death from cardiovascular or unknown causes. Key secondary outcomes included a microvascular composite endpoint, all-cause death, and heart failure. The effect of dulaglutide in patients with and without baseline metformin was evaluated by a Cox regression hazard model with baseline metformin, dulaglutide assignment, and their interaction as independent variables. Adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated by a Cox regression model with adjustments for factors differing at baseline between people with vs. without metformin, identified using the backward selection. RESULTS:Compared to patients with metformin at baseline (n = 8037; 81%), those without metformin (n = 1864; 19%) were older and slightly less obese and had higher proportions of women, prior CV events, heart failure, and renal disease. The primary outcome occurred in 976 (12%) participants with baseline metformin and in 281 (15%) without. There was no significant difference in the effect of dulaglutide on the primary outcome in patients with vs. without metformin at baseline [HR 0.92 (CI 0.81-1.05) vs. 0.78 (CI 0.61-0.99); interaction P = 0.18]. Findings for key secondary outcomes were similar in patients with and without baseline metformin. CONCLUSION:This analysis suggests that the cardioprotective effect of dulaglutide is unaffected by the baseline use of metformin therapy.

OBJECTIVE SENIOR compared the efficacy and safety of insulin glargine 300 units/mL (Gla-300) with glargine 100 units/mL (Gla-100) in older people (≥65 years old) with type 2 diabetes. RESEARCH DESIGN AND METHODS SENIOR was an open-label, two-arm, parallel-group, multicenter phase 3b trial designed to enroll ∼20% of participants aged ≥75 years. Participants were randomized 1:1 to Gla-300 or Gla-100, titrated to a fasting self-monitored plasma glucose of 5.0–7.2 mmol/L (90–130 mg/dL). RESULTS In total, 1,014 participants were randomized (mean age: 71 years). Comparable reductions in HbA1c were observed from baseline to week 26 for Gla-300 (−0.89%) and Gla-100 (−0.91%) in the overall population (least squares mean difference: 0.02% [95% CI −0.092 to 0.129]) and for participants aged ≥75 years (−0.11% [−0.330 to 0.106]). Incidence and rates of confirmed (≤3.9 mmol/L [≤70 mg/dL]) or severe hypoglycemia events were low and similar between both treatment groups, with lower rates of documented symptomatic hypoglycemia with Gla-300. The lower risk of hypoglycemia with Gla-300 versus Gla-100 was more apparent in the subgroup aged ≥75 years versus the overall population. Significantly lower annualized rates of documented symptomatic (≤3.9 mmol/L [≤70 mg/dL]) hypoglycemia were observed (Gla-300: 1.12; Gla-100: 2.71; rate ratio: 0.45 [95% CI 0.25–0.83]). CONCLUSIONS Efficacy and safety of Gla-300 was demonstrated in older people (≥65 years of age) with type 2 diabetes, with comparable reductions in HbA1c and similarly low or lower risk of documented symptomatic hypoglycemia versus Gla-100. A significant benefit in hypoglycemia reduction was seen in participants aged ≥75 years.

SENIOR war eine randomisierte, offene, zweiarmige, multizentrische, Phase-3b-Parallelgruppenstudie über 30 Wochen. Die Randomisierung wurde durch Abfragen des HbA1c (< 8,0 versus ≥8,0%), vorheriger Insulinanwendung (Ja/Nein) und Einnahme von Sulfonylharnstoffen oder Meglitinid (Ja/Nein) stratifiziert. Insulin wurde auf den von der ADA empfohlenen Blutzucker-Zielwert für gesunde ältere Menschen titriert (selbstgemessene Nüchtern-Plasmaglukose (SMPG): 90 – 130 mg/dl [5,0 – 7,2 mmol/l]); einen höheren Zielwert als der in vorherigen randomisierten kontrollierten Studien zu Insulin glargin 300 E/ml (Gla-300) versus 100 E/ml (Gla-100) bei Erwachsenen verwendete. Ziel der SENIOR-Studie war, Sicherheit und Wirksamkeit von Gla-300 versus Gla-100 zu vergleichen.

Both basal and postprandial elevations contribute to the hyperglycemic exposure of diabetes, but current therapies are mainly effective in controlling the basal component. Inability to control postprandial hyperglycemia limits success in maintaining overall glycemic control beyond the first 5 to 10 years after diagnosis, and it is also related to the weight gain that is common during insulin therapy. The "prandial problem" dcomprising abnormalities of glucose and other metabolites, weight gain, and risk of hypoglycemiaddeserves more attention. Several approaches to prandial abnormalities have recently been studied, but the patient populations forwhich they are best suited and the best ways of using them remain incompletely defined. Encouragingly, several proof-of-concept studies suggest that short-acting glucagon-like peptide 1 agonists or the amylin agonist pramlintide can be very effective in controlling postprandial hyperglycemia in type 2 diabetes in specific settings. This article reviews these topics and proposes that a greater proportion of available resources be directed to basic and clinical research on the prandial problem.

Both basal and postprandial elevations contribute to the hyperglycemic exposure of diabetes, but current therapies are mainly effective in controlling the basal component. Inability to control postprandial hyperglycemia limits success in maintaining overall glycemic control beyond the first 5 to 10 years after diagnosis, and it is also related to the weight gain that is common during insulin therapy. The "prandial problem"-comprising abnormalities of glucose and other metabolites, weight gain, and risk of hypoglycemia-deserves more attention. Several approaches to prandial abnormalities have recently been studied, but the patient populations for which they are best suited and the best ways of using them remain incompletely defined. Encouragingly, several proof-of-concept studies suggest that short-acting glucagon-like peptide 1 agonists or the amylin agonist pramlintide can be very effective in controlling postprandial hyperglycemia in type 2 diabetes in specific settings. This article reviews these topics and proposes that a greater proportion of available resources be directed to basic and clinical research on the prandial problem.

AimsInsulin glargine 300 U/mL (Gla‐300) offers a flatter pharmacodynamic profile than insulin glargine 100 U/mL (Gla‐100). We have compared these insulins over 1 year in people with type 1 diabetes (T1DM).Methods EDITION 4 was a 6‐month, multicentre, randomized, open‐label phase 3 study. People with T1DM who completed the 6 months continued randomized Gla‐300 or Gla‐100 once daily, morning or evening, for a further 6 months.ResultsAmong 549 participants randomized, 444 completed the 12‐month study period (Gla‐300, 80%; Gla‐100, 82%). Mean HbA1c decreased similarly from baseline to month 12 in the 2 treatment groups (difference, 0.02 [95% CI, −0.13 to 0.17]) %‐units [0.2 (−1.5 to 1.9) mmol/mol]), to a mean of 7.86 %‐units (62.4 mmol/mol) in both groups. For morning vs evening injection, there was no difference in HbA1c change over 12 months for Gla‐100, but a significantly larger decrease in HbA1c was observed in the Gla‐300 morning group than in the Gla‐300 evening group (difference, −0.25 [−0.47 to −0.04] %‐units [−2.7 (−5.2 to −0.4) mmol/mol]). Mean glucose from the 8‐point SMPG profiles decreased from baseline, and was similar between the 2 treatment groups. Basal insulin dose was 20% higher with Gla‐300 than with Gla‐100, while hypoglycaemia event rates, analysed at night, over 24 hours, or according to different glycaemic thresholds, did not differ between treatment groups, regardless of injection time. Adverse event profiles did not differ between groups.ConclusionsIn T1DM, Gla‐300 provides glucose control comparable to that of Gla‐100, and can be given at any time of day.

OBJECTIVEThe objective of this study was to compare glucose control in participants with type 1 diabetes receiving insulin glargine 300 units/mL (Gla-300) or glargine 100 units/mL (Gla-100) in the morning or evening, in combination with mealtime insulin.RESEARCH DESIGN AND METHODSIn this 16-week, exploratory, open-label, parallel-group, two-period crossover study (clinicaltrials.gov identifier NCT01658579), 59 adults with type 1 diabetes were randomized (1:1:1:1) to once-daily Gla-300 or Gla-100 given in the morning or evening (with crossover in the injection schedule). The primary efficacy end point was the mean percentage of time in the target glucose range (80-140 mg/dL), as measured using continuous glucose monitoring (CGM), during the last 2 weeks of each 8-week period. Additional end points included other CGM glycemic control parameters, hypoglycemia (per self-monitored plasma glucose [SMPG]), and adverse events.RESULTSThe percentage of time within the target glucose range was comparable between the Gla-300 and Gla-100 groups. There was significantly less increase in CGM-based glucose during the last 4 h of the 24-h injection interval for Gla-300 compared with Gla-100 (least squares mean difference -14.7 mg/dL [95% CI -26.9 to -2.5]; P = 0.0192). Mean 24-h glucose curves for the Gla-300 group were smoother (lower glycemic excursions), irrespective of morning or evening injection. Four metrics of intrasubject interstitial glucose variability showed no difference between Gla-300 and Gla-100. Nocturnal confirmed (<54 mg/dL by SMPG) or severe hypoglycemia rate was lower for Gla-300 participants than for Gla-100 participants (4.0 vs. 9.0 events per participant-year; rate ratio 0.45 [95% CI 0.24-0.82]).CONCLUSIONSLess increase in CGM-based glucose levels in the last 4 h of the 24-h injection interval, smoother average 24-h glucose profiles irrespective of injection time, and reduced nocturnal hypoglycemia were observed with Gla-300 versus Gla-100.

Background: Insulin glargine 300 U/mL (Gla-300) has a more constant and prolonged action profile than insulin glargine 100 U/mL and in clinical studies is associated with similar glycemic control but less hypoglycemia. Whether its effects are altered by variability of injection time was examined in two 3-month substudies.Materials and Methods: Eligible participants completing 6 months of optimized treatment with Gla-300 in EDITION 1 (n = 109) and EDITION 2 (n = 89), having a mean hemoglobin A1c (HbA(1c)) level of 7.3 % (SD 1.0 %), were randomized (1:1) to groups advised to increase variability of between-injection intervals to 24 +/- up to 3 h or to maintain fixed 24-h intervals for 3 months. Changes of HbA(1c) level and other efficacy and safety measures were assessed.Results: In the fixed-dosing group, 64% of participants reported all intervals within the 23-25-h range, compared with 15% of those advised flexible dosing. In the fixed- and flexible-dosing groups, 12% and 41%, respectively, of between-injection intervals were outside the 23-25-h range, and 2% and 16%, respectively, were outside the 21-27-h range. Least squares mean between-group difference in HbA(1c) change from baseline was 0.05 % (95% confidence interval [CI], -0.13 to 0.23); for fasting plasma glucose, 2.7 mg/dL (95% CI, -9.0 to 14.4); and for daily basal insulin dose, 0.00 U/kg (95% CI, -0.02 to 0.03). Frequencies of hypoglycemia and adverse events did not differ between groups.Conclusions: The efficacy and safety of Gla-300 demonstrated in EDITION 1 and EDITION 2 are maintained in substudies when the insulin was injected up to 3 h before or after the usual time of administration.

L'analyse poolée des études EDITION 1, 2 et 3 (sur 6 mois), a montré que l'insuline glargine 300 U/mL (Gla-300) provoquait moins d'hypoglycémies confirmées ou sévères (soit nocturnes, de 00 h 00 à 05 h 59, soit sur l'ensemble des 24 h) que l'insuline glargine 100 U/mL (Gla-100) chez des patients DT2. Cependant, cette fenêtre nocturne théorique ne reflète généralement pas de manière appropriée la période de jeûne nocturne. Une analyse plus fine a permis de définir l'exposition nocturne comme allant de 22 h 00 à l'auto-données étaient disponibles pour 2 488 patients [population randomisée (N = 2 496), âge moyen 59 ans, durée du diabète 13 ans, IMC 35 kg/m2]. L'heure moyenne du petit-déjeuner était 07 h 30 (écart interquartile : 07 h 00 – 08 h 19). La période ainsi définie comprenait plus d'événements hypoglycémiques que la fenêtre 00 h 00 – 05 h 59 (Gla-300 3 585 vs 1 235 ; Gla-100 4 730 vs 1 791). Le pourcentage de patients ayant ≥ 1 épisode était plus faible avec Gla-300 qu'avec Gla-100 quelle que soit la définition (risque relatif = ,75 (0,68 à 0,83) de 00 h 00 à 05 h 59 et 0,84 (0,78 à 0,89) dans la fenêtre définie cliniquement). Les taux d'événements/année étaient aussi plus faibles avec Gla-300 qu'avec Gla-100, selon les deux définitions (rapport de taux 31 % plus bas de 00 h 00 à 05 h 59 ; 24 % dans la fenêtre définie cliniquement). La différence absolue du nombre d'épisodes (en faveur de Gla-300) était plus grande dans la fenêtre cliniquement définie (1 145 vs 556). Le bénéfice de Gla-300 sur Gla-100 en termes d'hypoglycémies nocturnes est confirmé avec les deux définitions. La diminution relative du pourcentage des patients concernés et du taux d'épisodes était plus importante de 00 h 00 à 05 h 59, mais la réduction du nombre absolu d'épisodes sous Gla-300 pendant la période nocturne définie cliniquement est certainement d'une plus grande pertinence clinique. Étude sponsorisée par Sanofi Abstract original publié à l'ADA 2015. Riddle MC, et al. Diabètes 2015 ; 64 (suppl 1) : A263 [Abstract 1027-P]

Achieving near-normal glucose homeostasis infers that all components of dysglycemia that are present in diabetic states should be eradicated. At present, there is incontrovertible evidence that controlling chronic glucose exposure exerts consistent benefit on the incidence of all related diabetes complications (1,2). However, we are sadly lacking similar evidence for implicating glucose variability (GV) as an independent causative factor for vascular complications in those with diabetes. In an attempt to answer this question, the investigators of the FLuctuATion reduction with inSUlin and GLP-1 Added togetheR (FLAT-SUGAR) trial (3) have randomly assigned patients with insulin-requiring type 2 diabetes to two basal-prandial therapeutic protocols. The first one was the classic basal-bolus insulin …

Comparer la nouvelle insuline glargine 300 U/ml (Gla-300) vs l'insuline glargine 100 U/ml (Gla-100) sur le contrôle glycémique de patients diabétiques de type 2 (DT2) traités par insuline basale et antidiabétiques oraux (ADO). Huit cent onze patients adultes DT2 ayant un contrôle insuffisant d'HbA1c ont été randomisés pour recevoir Gla-300 (n = 403, HbA1c 8,26 ± 0,86 %) ou Gla-100 (n = 405, HbA1c 8,21 ± 0,77 %) pendant 6 mois. Au cours d'une prolongation en ouvert de 6 mois, les participants ont continué à recevoir Gla-300 ou Gla-100 une fois par jour, en association avec des ADO ; 315 (78 %) de participants sous Gla-300 et 314 (77 %) de participants sous Gla-100 ont complété les 12 mois de traitement. Après 12 mois de suivi, l'abaissement du taux d'HbA1c était similaire: – 0,55 (– 0,67 à – 0,44) avec Gla-300 vs – 0,5 (– 0,61 à – 0,39) avec Gla-100. Sur les 12 mois de traitement, le taux d'hypoglycémies nocturnes confirmées (≤ 70 mg/dl) ou sévères était de 37 % inférieur sous Gla-300, que sous Gla-100 (1,74 vs 2,77 épi-sodes/années patients, RR = 0,63 [IC 95 % = 0,42-0,96]). Moins de participants ont présenté ≥ 1 épisode d'hypoglycémie nocturne confirmé ou sévère sous Gla-300 que sous Gla-100 (RR = 0,84 [IC 95 % = 0,71-0,99]). L'hypoglycémie sévère à tout moment de la journée était rare: 7 patients du groupe Gla-300 et 6 du groupe Gla-100. Une augmentation pondérale a été observée dans les deux groupes, mais était significativement moins importante dans le groupe Gla-300 que dans le groupe Gla-100 (moyennes par moindres carrés [IC 95 %] = 0,42 kg [0,04-0,80] vs 1,14 kg [0,76- 1,52], p = 0,0091). L'incidence des événements indésirables a été comparable dans les deux groupes de traitement. Au cours des 12 mois de suivi, les patients DT2 traités par Gla-300 + ADO ont eu un contrôle glycémique équivalent à ceux utilisant Gla-100 + ADO, avec moins d'épisodes d'hypoglycémies nocturnes et moins de prise de poids. Étude financée par Sanofi (NCT01499095) Les auteurs déclarent avoir un intérêt avec un organisme privé, industriel ou commercial en relation avec le sujet présenté. Étude financée par Sanofi (NCT01499095).

Comparer les profils glycémiques de patients diabétiques de type 1 (DT1) traités par insuline glargine 300 U/ml (Gla-300) ou 100 U/ml (Gla-100) à l’aide d’enregistrements glycémiques continus (CGMS). Étude multicentrique de 16 semaines, en ouvert. 59 DT1 adultes (âge moyen 44,2 ans, durée du diabète 22,1 ans ; HbA1c 7,46 %) ont été randomisés (1 : 1) en deux groupes (Gla-300 ou Gla-100 injectées une fois/j, le matin ou le soir en crossover). Le taux d’HbA1c à 16 semaines et la glycémie moyenne des 2 dernières semaines, mesurée par le capteur-CGMS (CG), étaient similaires dans les groupes Gla-300 (7,02 % et 9,2 mmol/L) et Gla-100 (7,17 % et 9,4 mmol/L). Le pourcentage de temps passé dans l’intervalle glycémique cible de 4,4 à 7,8 mmol/L était de 32 % avec Gla-300 vs 31 % avec Gla-100 (NS). Le temps passé avec des valeurs sous des différents seuils d’hypoglycémie (3,9, 3,3, 2,8 et 2,2 mmol/L) ou au-dessus des seuils d’hyperglycémie (10,0, 13,9 et 22,2 mmol/L) était moindre dans le groupe Gla-300 vs Gla-100. Les fréquences (%) des valeurs (GC) < 3,3 mmol/L et > 13,9 mmol/L pour les patients sous Gla-300 vs Gla-100 étaient (moy. ± SD) : 4,7 ± 3,3 vs 5,4 ± 4,3 et 12,7 ± 8,0 vs 16,4 ± 10,5 respectivement. Les profils glycémiques sur 24 heures ont révélé moins d’excursions glycémiques avec la Gla-300. Lorsque les périodes d’injection (matin et soir) ont été combinées, tous les paramètres individuels de variabilité glycémique ont été significativement inférieurs avec la Gla-300 (écart-type total = 7,4 %, variabilité intrajournalière = – 5,4 %, variabilité entre les moyennes journalières = – 14,3 % et variabilité interjournalière = – 7,2 %). Sous Gla-300 et Gla-100 le contrôle glycémique moyen et la durée globale de maintien dans les valeurs cibles (4,4-7,8 mmol/L) sont similaires, mais la fréquence des hypoglycémies et des excursions glycémiques, ainsi que la variabilité glycémique intra- et interjournalière, sont moindres sous Gla-300. Étude financée par Sanofi (NCT01658579) Les auteurs déclarent avoir un intérêt avec un organisme privé, industriel ou commercial en relation avec le sujet présenté. Étude financée par Sanofi (NCT01658579).