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Insulin Aspart Sanofi, If It Is Coloured Or It Has Solid Pieces in It
ANNEX I SUMMARY OF PRODUCT CHARACTERISTICS 1 This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse reactions. See section 4.8 for how to report adverse reactions. 1. NAME OF THE MEDICINAL PRODUCT Insulin aspart Sanofi 100 units/ml solution for injection in vial Insulin aspart Sanofi 100 units/ml solution for injection in cartridge Insulin aspart Sanofi 100 units/ml solution for injection in pre-filled pen 2. QUALITATIVE AND QUANTITATIVE COMPOSITION One ml solution contains 100 units insulin aspart* (equivalent to 3.5 mg). Insulin aspart Sanofi 100 units/ml solution for injection in vial Each vial contains 10 ml equivalent to 1,000 units insulin aspart. Insulin aspart Sanofi 100 units/ml solution for injection in cartridge Each cartridge contains 3 ml equivalent to 300 units insulin aspart. Insulin aspart Sanofi 100 units/ml solution for injection in pre-filled pen Each pre-filled pen contains 3 ml equivalent to 300 units insulin aspart. Each pre-filled pen delivers 1-80 units in steps of 1 unit. *produced in Escherichia coli by recombinant DNA technology. For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM Solution for injection (injection). Clear, colourless, aqueous solution. 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Insulin aspart Sanofi is indicated for the treatment of diabetes mellitus in adults, adolescents and children aged 1 year and above. 4.2 Posology and method of administration Posology The potency of insulin analogues, including insulin aspart, is expressed in units, whereas the potency of human insulin is expressed in international units. -
Combining a Glucagon-Like Peptide-1 Receptor Agonist with Basal Insulin: the Why and How
Combining a Glucagon-like Peptide-1 Receptor Agonist with Basal Insulin: The Why and How Case Study Mary is a 61 year-old female diagnosed with type 2 diabetes mellitus (T2DM) 8 years ago. She was initially managed with the combination of lifestyle modification and metformin. Since that time she was treated with a sulfonylurea, but it was discontinued due to symptomatic hypoglycemia. She was also treated with pioglitazone, but significant fluid retention led to it discontinuation. A year-and-a- half ago, basal insulin was added to her lifestyle and metformin management. She now administers 52 units (0.62 units/kg) once daily at bedtime. Since starting basal insulin, she has experienced 3 episodes of mild hypoglycemia. Since her diagnosis, Mary’s HbA1c has never been <7.0%; her current HbA1c is 7.9%. Over the past month, her fasting plasma glucose (FPG) has ranged from 103 mg/dL to 136 mg/dL and her postprandial glucose (PPG) from 164 mg/dL to 213 mg/dL. She has gained 2.6 kg since starting basal insulin and her body mass index is now 31 kg/m2. Her blood pressure is 134/82 mmHg. She experiences occasional tingling in her feet. Eye examination reveals grade 1 retinopathy. Current medications are: metformin 1000mg twice daily, basal insulin 52 units once daily at bedtime, and hydrochlorothiazide 25 mg once daily. Her family physician notes that Mary’s FPG is reasonably well-controlled, yet her HbA1c and PPG remain elevated. He is also concerned about her episodes of hypoglycemia and weight gain and the evidence indicating microvascular damage. -
(Pram) and Insulin A21G Improves Post-Prandial Glucose Vs Novolog
ADO09, A Co-Formulation Of Pramlintide (Pram) and Insulin A21G improves Post-Prandial Glucose Vs Novolog® in Type 1 Diabetes (T1DM) G.Meiffren¹, G.Andersen², R.Eloy¹, C.Seroussi¹, C.Mégret¹, S.Famulla², Y.-P Chan¹, M.Gaudier¹, O.Soula¹, J.H. DeVries²,T.Heise² (1 Adocia, Lyon, France ; 2 Profil, Neuss, Germany) Introduction & Background Overall safety Outpatient period results - CGM metrics o ADO09 (M1Pram) is a co-formulation of pramlintide and insulin A21G o Both treatments were well tolerated without any treatment-related serious adverse events o Most of the CGM metrics (TiR [70-180], TiR [80-140], mean blood glucose per day), were significantly improved developed to leverage the beneficial effects of pramlintide on post-prandial (Table 2). As expected M1Pram had numerically more, mostly gastrointestinal adverse events with M1Pram (Table 4). Postprandial and mean 24-hour glucose profiles were improved with M1Pram (Fig. 3) glucose without additional injections than insulin aspart Table 4: CGM metrics, all days. Significant differences are marked in bold Objective and design o No severe hypoglycemia were seen, slightly more hypoglycemic events occurred with M1Pram Ratio of LSMean* o To compare the effect of M1Pram and insulin aspart (Novolog®, Novo than with aspart (Table 3) Difference Parameter Treatment LS Mean M1Pram / Aspart P-value Nordisk) on post-prandial glucose control, glycemic control assessed by Table 2: Incidence of adverse events throughout the trial (M1Pram-Aspart) (95% CI) CGM and safety/tolerability M1Pram Aspart M1Pram -
Comparative Transcriptional Network Modeling of Three PPAR-A/C Co-Agonists Reveals Distinct Metabolic Gene Signatures in Primary Human Hepatocytes
Comparative Transcriptional Network Modeling of Three PPAR-a/c Co-Agonists Reveals Distinct Metabolic Gene Signatures in Primary Human Hepatocytes Rene´e Deehan1, Pia Maerz-Weiss2, Natalie L. Catlett1, Guido Steiner2, Ben Wong1, Matthew B. Wright2*, Gil Blander1¤a, Keith O. Elliston1¤b, William Ladd1, Maria Bobadilla2, Jacques Mizrahi2, Carolina Haefliger2, Alan Edgar{2 1 Selventa, Cambridge, Massachusetts, United States of America, 2 F. Hoffmann-La Roche AG, Basel, Switzerland Abstract Aims: To compare the molecular and biologic signatures of a balanced dual peroxisome proliferator-activated receptor (PPAR)-a/c agonist, aleglitazar, with tesaglitazar (a dual PPAR-a/c agonist) or a combination of pioglitazone (Pio; PPAR-c agonist) and fenofibrate (Feno; PPAR-a agonist) in human hepatocytes. Methods and Results: Gene expression microarray profiles were obtained from primary human hepatocytes treated with EC50-aligned low, medium and high concentrations of the three treatments. A systems biology approach, Causal Network Modeling, was used to model the data to infer upstream molecular mechanisms that may explain the observed changes in gene expression. Aleglitazar, tesaglitazar and Pio/Feno each induced unique transcriptional signatures, despite comparable core PPAR signaling. Although all treatments inferred qualitatively similar PPAR-a signaling, aleglitazar was inferred to have greater effects on high- and low-density lipoprotein cholesterol levels than tesaglitazar and Pio/Feno, due to a greater number of gene expression changes in pathways related to high-density and low-density lipoprotein metabolism. Distinct transcriptional and biologic signatures were also inferred for stress responses, which appeared to be less affected by aleglitazar than the comparators. In particular, Pio/Feno was inferred to increase NFE2L2 activity, a key component of the stress response pathway, while aleglitazar had no significant effect. -
Lobeglitazone
2013 International Conference on Diabetes and Metabolism Lobeglitazone, A Novel PPAR-γ agonist with balanced efficacy and safety Kim, Sin Gon. MD, PhD. Professor, Division of Endocrinology and Metabolism Department of Internal Medicine, Korea University College of Medicine. Disclosure of Financial Relationships This symposium is sponsored by Chong Kun Dang Pharmaceutical Corp. I have received lecture and consultation fees from Chong Kun Dang. Pros & Cons of PPAR-γ agonist Pros Cons • Good glucose lowering • Adverse effects • Durability (ADOPT) (edema, weight gain, • Insulin sensitizing CHF, fracture or rare effects (especially in MS, macular edema etc) NAFLD, PCOS etc) • Possible safety issues • Prevention of new- (risk of MI? – Rosi or onset diabetes (DREAM, bladder cancer? - Pio) ACT-NOW) • LessSo, hypoglycemiathere is a need to develop PPAR-γ • Few GI troubles agonist• Outcome with data balanced efficacy and safety (PROactive) Insulin Sensitizers : Several Issues Rosi, Peak sale ($3.3 billion) DREAM Dr. Nissen Dr. Nissen ADOPT META analysis BARI-2D (5,8) Rosi, lipid profiles RECORD 1994 1997 1999 2000 2002 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 Tro out d/t FDA, All diabetes hepatotoxicity drug CV safety Rosi (5) FDA, Black box Rosi, Rosi , CV safety warning - REMS in USA = no evidence - Europe out Pio (7) PIO, bladder cancer CKD 501 Lobeglitazone 2000.6-2004.6 2004.11-2007.1 2007.3-2008.10 2009.11-2011.04 Discovery& Preclinical study Phase I Phase II Phase III Developmental Strategy Efficacy • PPAR activity Discovery & Preclinical study • In vitro & vivo efficacy • Potent efficacy 2000.06 - 2004.06 Phase I 2004.11 - 2007.01 • In vitro screening • Repeated dose toxicity • Metabolites • Geno toxicity • Phase II CYP 450 • Reproductive toxicity 2007.03 - 2008.10 • DDI • Carcinogenic toxicity ADME Phase III Safety 2009.11 - 2011.04 CV Safety / (Bladder) Cancer / Liver Toxicity / Bone loss Lobeglitazone (Duvie) 1. -
Title: Combination of Pparg Agonist Pioglitazone and Trabectedin Induce Adipocyte Differentiation to Overcome Trabectedin Resistance in Myxoid Liposarcomas
Author Manuscript Published OnlineFirst on September 3, 2019; DOI: 10.1158/1078-0432.CCR-19-0976 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Title: Combination of PPARg agonist pioglitazone and trabectedin induce adipocyte differentiation to overcome trabectedin resistance in myxoid liposarcomas Roberta Frapolli1, Ezia Bello1, Marianna Ponzo1, Ilaria Craparotta2, Laura Mannarino2, Sara Ballabio2, Sergio Marchini2, Laura Carrassa3, Paolo Ubezio4, Luca Porcu5, Silvia Brich6, Roberta Sanfilippo7, Paolo Giovanni Casali7, Alessandro Gronchi8, Silvana Pilotti6, and Maurizio D’Incalci9*. 1 Unit of Preclinical Experimental Therapeutics, Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy. 2 Unit of Translational Genomic, Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy. 3Unit of DNA repair, Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy. 4 Unit of Biophysics, Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy. 5 Unit of Methodological Research, Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy. 6Laboratory of Molecular Pathology, Department of Pathology, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. 7 Medical Oncology Unit 2, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. 8 Department of Surgery, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. 9 Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, 20156 Milan, Italy. Running title: Pioglitazone - trabectedin in myxoid liposarcomas. Keywords: Myxoid liposarcoma, trabectedin resistance, PPAR agonist, and patient-derived xenograft. Additional information: Financial support: This work was supported by the Italian Association for Cancer Research grant to M.D. -
Type 2 Diabetes Adult Outpatient Insulin Guidelines
Diabetes Coalition of California TYPE 2 DIABETES ADULT OUTPATIENT INSULIN GUIDELINES GENERAL RECOMMENDATIONS Start insulin if A1C and glucose levels are above goal despite optimal use of other diabetes 6,7,8 medications. (Consider insulin as initial therapy if A1C very high, such as > 10.0%) 6,7,8 Start with BASAL INSULIN for most patients 1,6 Consider the following goals ADA A1C Goals: A1C < 7.0 for most patients A1C > 7.0 (consider 7.0-7.9) for higher risk patients 1. History of severe hypoglycemia 2. Multiple co-morbid conditions 3. Long standing diabetes 4. Limited life expectancy 5. Advanced complications or 6. Difficult to control despite use of insulin ADA Glucose Goals*: Fasting and premeal glucose < 130 Peak post-meal glucose (1-2 hours after meal) < 180 Difference between premeal and post-meal glucose < 50 *for higher risk patients individualize glucose goals in order to avoid hypoglycemia BASAL INSULIN Intermediate-acting: NPH Note: NPH insulin has elevated risk of hypoglycemia so use with extra caution6,8,15,17,25,32 Long-acting: Glargine (Lantus®) Detemir (Levemir®) 6,7,8 Basal insulin is best starting insulin choice for most patients (if fasting glucose above goal). 6,7 8 Start one of the intermediate-acting or long-acting insulins listed above. Start insulin at night. When starting basal insulin: Continue secretagogues. Continue metformin. 7,8,20,29 Note: if NPH causes nocturnal hypoglycemia, consider switching NPH to long-acting insulin. 17,25,32 STARTING DOSE: Start dose: 10 units6,7,8,11,12,13,14,16,19,20,21,22,25 Consider using a lower starting dose (such as 0.1 units/kg/day32) especially if 17,19 patient is thin or has a fasting glucose only minimally above goal. -
OSENI Safely and Effectively
HIGHLIGHTS OF PRESCRIBING INFORMATION -----------------------WARNINGS AND PRECAUTIONS---------------------- These highlights do not include all the information needed to use Congestive heart failure: Fluid retention may occur and can OSENI safely and effectively. See full prescribing information for exacerbate or lead to congestive heart failure. Combination use OSENI. with insulin and use in congestive heart failure NYHA Class I and OSENI (alogliptin and pioglitazone) tablets II may increase risk. Monitor patients for signs and symptoms. Initial U.S. Approval: 2013 (5.1) Acute pancreatitis: There have been postmarketing reports of WARNING: CONGESTIVE HEART FAILURE acute pancreatitis. If pancreatitis is suspected, promptly See full prescribing information for complete boxed warning discontinue OSENI. (5.2) Thiazolidinediones, including pioglitazone, cause or Hypersensitivity: There have been postmarketing reports of exacerbate congestive heart failure in some patients. (5.1) serious hypersensitivity reactions in patients treated with alogliptin After initiation of OSENI and after dose increases, monitor such as anaphylaxis, angioedema and severe cutaneous adverse patients carefully for signs and symptoms of heart failure reactions. In such cases, promptly discontinue OSENI, assess for (e.g., excessive, rapid weight gain, dyspnea, and/or other potential causes, institute appropriate monitoring and edema). If heart failure develops, it should be managed treatment, and initiate alternative treatment for diabetes. (5.3) according to current standards of care and Hepatic effects: Postmarketing reports of hepatic failure, discontinuation or dose reduction of pioglitazone in OSENI sometimes fatal. Causality cannot be excluded. If liver injury is must be considered. detected, promptly interrupt OSENI and assess patient for OSENI is not recommended in patients with symptomatic probable cause, then treat cause if possible, to resolution or heart failure. -
New Diabetes Medications: Where Do They Fit in the Paradigm?
NEW DIABETES MEDICATIONS: WHERE DO THEY FIT IN THE PARADIGM? Nabila Ahmed-Sarwar, Pharm.D., BCPS, CDE Elizabeth Sutton Burke, Pharm.D., BCACP, CDE Wegmans School of Pharmacy November 19 th , 2016 Disclosure Statement No relevant financial relationships to disclose Learning Objectives Upon completion of this educational session, participants will be able to: • Summarize current and new targets for drug action that influence glucose homeostasis • Explain the clinical impact of the new therapeutic agents and determine their place in therapy for the treatment of diabetes mellitus Current Treatment Options Location Medications Effect Secretagogues Increase serum insulin DPP-IV Inhibitors levels Insulin Metformin Decrease Thiazolidinediones gluconeogenesis Increase glucose uptake Alpha-glucosidase Decrease glucose Inhibitors absorption Pramlintide American Diabetes Association-Standards of Care. Diabetes Care 2016 Where do we go from here?? Improved Improved Safety Efficacy Alternative Desirable targets for Administration glucose Regimens homeostasis New Anti-hyperglycemic Agents New Treatment Options Location Medications Effect Increase serum insulin levels Basal Insulins GLP-1 Analogs Decrease glucagon release SGLT-2 Inhibitors Increase urinary glucose excretion Where do we go from here?? Improved Improved Safety Efficacy Alternative Desirable targets for Administration glucose Regimens homeostasis New Anti-hyperglycemic Agents Basal-Rapid Acting Regimen Provides continuous basal coverage Insulin 7 amnoon 7 pm 11 pm 7 am Basal Insulins Generic -
Muraglitazar Bristol-Myers Squibb/Merck Daniella Barlocco
Muraglitazar Bristol-Myers Squibb/Merck Daniella Barlocco Address Originator Bristol-Myers Squibb Co University of Milan . Istituto di Chimica Farmaceutica e Tossicologica Viale Abruzzi 42 Licensee Merck & Co Inc 20131 Milano . Italy Status Pre-registration Email: [email protected] . Indications Metabolic disorder, Non-insulin-dependent Current Opinion in Investigational Drugs 2005 6(4): diabetes © The Thomson Corporation ISSN 1472-4472 . Actions Antihyperlipidemic agent, Hypoglycemic agent, Bristol-Myers Squibb and Merck & Co are co-developing Insulin sensitizer, PPARα agonist, PPARγ agonist muraglitazar, a dual peroxisome proliferator-activated receptor-α/γ . agonist, for the potential treatment of type 2 diabetes and other Synonym BMS-298585 metabolic disorders. In November 2004, approval was anticipated as early as mid-2005. Registry No: 331741-94-7 Introduction [579218], [579221], [579457], [579459]. PPARγ is expressed in Type 2 diabetes is a complex metabolic disorder that is adipose tissue, lower intestine and cells involved in characterized by hyperglycemia, insulin resistance and immunity. Activation of PPARγ regulates glucose and lipid defects in insulin secretion. The disease is associated with homeostasis, and triggers insulin sensitization [579216], older age, obesity, a family history of diabetes and physical [579218], [579458], [579461]. PPARδ is expressed inactivity. The prevalence of type 2 diabetes is increasing ubiquitously and has been found to be effective in rapidly, and the World Health Organization warns that, controlling dyslipidemia and cardiovascular diseases unless appropriate action is taken, the number of sufferers [579216]. PPARα agonists are used as potent hypolipidemic will double to over 350 million individuals by the year compounds, increasing plasma high-density lipoprotein 2030. Worryingly, it is estimated that only half of sufferers (HDL)-cholesterol and reducing free fatty acids, are diagnosed with the condition [www.who.int]. -
Glucagon-Like Peptide-1 Receptor Agonists
Clinical Policy: Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists Reference Number: HIM.PA.53 Effective Date: 03.01.18 Last Review Date: 02.21 Line of Business: HIM Revision Log See Important Reminder at the end of this policy for important regulatory and legal information. Description The following agents contain a synthetic glucagon-like peptide-1 (GLP-1) receptor agonist and require prior authorization: dulaglutide (Trulicity®), exenatide ER (Bydureon®, Bydureon BCise®), exenatide IR (Byetta®), liraglutide (Victoza®), liraglutide/insulin degludec (Xultophy®), lixisenatide (Adlyxin®), lixisenatide/insulin glargine (Soliqua®), and semaglutide (Ozempic®, Rybelsus®). FDA Approved Indication(s) GLP-1 receptor agonists are indicated as adjunct to diet and exercise to improve glycemic control with type 2 diabetes mellitus. Victoza is indicated in patients 10 years of age and older, while the other GLP-1 receptor agonists are indicated in adults. Ozempic, Trulicity and Victoza are also indicated to reduce the risk of major adverse cardiovascular events in adults with type 2 diabetes mellitus and: • Established cardiovascular disease (Ozempic, Trulicity, Victoza); • Cardiovascular risk factors (Trulicity only). Limitation(s) of use: • Trulicity, Bydureon, Bydureon BCise, and Xultophy are not recommended as a first-line therapy for patients inadequately controlled on diet and exercise. • Other than Soliqua and Xultophy which contains insulin, GLP-1 receptor agonists are not a substitute for insulin. They should not be used for the treatment of type 1 diabetes or diabetic ketoacidosis. • Other than Trulicity, concurrent use with prandial insulin has not been studied and cannot be recommended. • GLP-1 receptor agonists have not been studied in patients with a history of pancreatitis. -
Tresiba-Product-Monograph.Pdf
PRODUCT MONOGRAPH INCLUDING PATIENT MEDICATION INFORMATION TRESIBA® insulin degludec injection TRESIBA® FlexTouch® 100 U/mL, Solution for injection in a pre-filled pen TRESIBA® FlexTouch® 200 U/mL, Solution for injection in a pre-filled pen Subcutaneous Antidiabetic Agent Long-Acting Basal Insulin Analogue ATC Code: A10AE06 Novo Nordisk Canada Inc. Date of Initial Authorization: AUG 25, 2017 101-2476 Argentia Road Date of Revision: Mississauga, Ontario JUL 23, 2021 Canada L5N 6M1 Submission Control Number: 250276 Product Monograph Master Template Template Date: September 2020 TRESIBA® (insulin degludec injection) Page 1 of 2 RECENT MAJOR LABEL CHANGES 7 Warnings and Precautions 03/2021 TABLE OF CONTENTS Sections or subsections that are not applicable at the time of authorization are not listed. TABLE OF CONTENTS ..............................................................................................................2 1 INDICATIONS ..................................................................................................................4 1.1 Pediatrics ................................................................................................................4 1.2 Geriatrics ................................................................................................................4 2 CONTRAINDICATIONS ..................................................................................................4 3 SERIOUS WARNINGS AND PRECAUTIONS BOX .......................................................4 4 DOSAGE AND ADMINISTRATION