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SUBMITTED BY : BUNTI SINGHAL
M.PHARMACY (PH.COLOGY)
INSTITUTE OF PHARMACEUTICAL SCIENCE
KURUKSHETRA UNIVERSITY
 Chronic metabolic disorder characterised by
persistent high blood glucose concentration.
 Cause: insulin deficiency or insulin resistance.
 Types:
1. DM Type1:Juvenile onset (insulin dependent)
2. DM Type2:tissue insensitivity.
S
Y
M
P
T
O
M
S
1.NON PHARMACOLOGICAL
 Weight loss
 Regular physical activity
 Lifestyle changes
2.INSULIN
 Rapid acting- lispro, aspart
 Short acting- regular
 Intermediate acting- NPH, lente
 Long acting- ultra lente, protamine zinc
3.ORAL HYPOGLYCEMIC DRUGS
 Insulin secretagogeous :
a. Sulphonyl urea: tolbutamide, clibenclamide
b. Meglitinide: rapeglinide, nateglinide
 Insulin sensitizers :
a. Biguanides : metformin, phenformin
b. TZDs(PPAR) : rosiglitazone, pioglitazone
 alpha glucosidase inhibitors :
acarbose, miglitol, voglibose
 Insulin discovered in 1922 by Banting and
Best. Abel isolated in crystalline state.
 Secreted by beta cells of pancreas.
 Polypeptide consist of 2 peptide chain
connected by two disulphide bridges.
 WHY NEWER INSULIN ?
 -Lipodystrophy
 -Insulin allergy
 -Antibody related resistance
 -hypoglycemia
DETEMIR DEGLUDEC
Available as LEVEMIR FLEXPEN®
Hypoglycemia less frequent
Less nocturnal hypoglucemia
Less or minimal weight gain
T1/2 25TO 40 hrs
Administered any time of day
Can be mixed with other insulin
Effect at physiological ph.
1.LONG ACTING INSULIN ANALOGUE:
2.HEXYL-INSULIN MONOCONJUGATE-2(HIM-2)
 Modified oral human insulin.
 Enhance stability, resistant to intestinal degradation.
 Absorbed from GIT directly into portal circulation.
3.ORAL INSULIN SPRAY FORMULATION
 Oral-lyn™
 Faster onset & short duration
4.INHALATIONAL INSULIN
 Available in powder form
 Absorption from lungs
EXUBERA
AFREZZA
5.NEWER INSULIN DELIVERY SYSTEM
i. INSULIN PUMP:Continuous SC insulin
infusion (CSII)
ii. PEN DEVICES
INSULIN PUMP INSULIN PEN
WHY NEWER DRUGS ?
• Adverse effect profile:
-unacceptable weight gain
-abdominal distention & flatulence
with acarbose.
• Basic pathology is left unaltered.
-no strategy available to protect
beta cells
NEWER DRUGS
1.Newer Insulins
2.Incretin-based therapy:
GLP-1 analogues: Exenatide, Liraglutide
DPP 4 inhibitors: Sitagliptin, Vidagliptin
3.Amylin analogue: Pramlintide
4.Dual PPAR agonists: Aleglitazar,
Muraglitazar, Tesaglitazar
5.SGLT2 inhibitors: Dapagliflozin,
canagliflozin, empagliflozin
6.Others: Bromocriptine
1.Incretin-based therapy: GIT HORMONE
GLP1 ANALOGUE DPP4 INHIBITORS
• Insulin secretion
• Glucose uptake
• Gastric emptying
• Glucose production
• e.g.exenatide, liraglutide
• Level of GLP1 & GIP
• e.g.sitagliptin, vildagliptin
2.AMYLIN ANALOGUE: amylin is secreted from
beta cells.(PRAMLINTIDE)
3.DUAL PPAR AGONIST: Aleglitazar,
Muraglitazar, Tesaglitazar
• Supress glucagon production
• Reduce hepatic glucose production
• Delay gastric emptying
PPAR ALPHA PPAR GAMA
(LIVER, VASCULAR WALL)
• Inc. circulating HDL
• Reduce triglycerides
(FAT, MUSCLE)
• Modulate glucose
metabolism.
4.SGLT2 INHIBITORS: DAPAGLIFLOZIN,
CANAGLIFLOZIN,EMPAGLIFLOZIN.
• Express in proximal tubule of kidney
• Inhibition of glucose reabsorption.
INDIA

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Recent advancement in treatment of diabetes mellitus

  • 1. SUBMITTED BY : BUNTI SINGHAL M.PHARMACY (PH.COLOGY) INSTITUTE OF PHARMACEUTICAL SCIENCE KURUKSHETRA UNIVERSITY
  • 2.  Chronic metabolic disorder characterised by persistent high blood glucose concentration.  Cause: insulin deficiency or insulin resistance.  Types: 1. DM Type1:Juvenile onset (insulin dependent) 2. DM Type2:tissue insensitivity. S Y M P T O M S
  • 3. 1.NON PHARMACOLOGICAL  Weight loss  Regular physical activity  Lifestyle changes 2.INSULIN  Rapid acting- lispro, aspart  Short acting- regular  Intermediate acting- NPH, lente  Long acting- ultra lente, protamine zinc
  • 4. 3.ORAL HYPOGLYCEMIC DRUGS  Insulin secretagogeous : a. Sulphonyl urea: tolbutamide, clibenclamide b. Meglitinide: rapeglinide, nateglinide  Insulin sensitizers : a. Biguanides : metformin, phenformin b. TZDs(PPAR) : rosiglitazone, pioglitazone  alpha glucosidase inhibitors : acarbose, miglitol, voglibose
  • 5.  Insulin discovered in 1922 by Banting and Best. Abel isolated in crystalline state.  Secreted by beta cells of pancreas.  Polypeptide consist of 2 peptide chain connected by two disulphide bridges.  WHY NEWER INSULIN ?  -Lipodystrophy  -Insulin allergy  -Antibody related resistance  -hypoglycemia
  • 6.
  • 7. DETEMIR DEGLUDEC Available as LEVEMIR FLEXPEN® Hypoglycemia less frequent Less nocturnal hypoglucemia Less or minimal weight gain T1/2 25TO 40 hrs Administered any time of day Can be mixed with other insulin Effect at physiological ph. 1.LONG ACTING INSULIN ANALOGUE: 2.HEXYL-INSULIN MONOCONJUGATE-2(HIM-2)  Modified oral human insulin.  Enhance stability, resistant to intestinal degradation.  Absorbed from GIT directly into portal circulation.
  • 8. 3.ORAL INSULIN SPRAY FORMULATION  Oral-lyn™  Faster onset & short duration 4.INHALATIONAL INSULIN  Available in powder form  Absorption from lungs EXUBERA AFREZZA
  • 9. 5.NEWER INSULIN DELIVERY SYSTEM i. INSULIN PUMP:Continuous SC insulin infusion (CSII) ii. PEN DEVICES INSULIN PUMP INSULIN PEN
  • 10. WHY NEWER DRUGS ? • Adverse effect profile: -unacceptable weight gain -abdominal distention & flatulence with acarbose. • Basic pathology is left unaltered. -no strategy available to protect beta cells
  • 11. NEWER DRUGS 1.Newer Insulins 2.Incretin-based therapy: GLP-1 analogues: Exenatide, Liraglutide DPP 4 inhibitors: Sitagliptin, Vidagliptin 3.Amylin analogue: Pramlintide 4.Dual PPAR agonists: Aleglitazar, Muraglitazar, Tesaglitazar 5.SGLT2 inhibitors: Dapagliflozin, canagliflozin, empagliflozin 6.Others: Bromocriptine
  • 12. 1.Incretin-based therapy: GIT HORMONE GLP1 ANALOGUE DPP4 INHIBITORS • Insulin secretion • Glucose uptake • Gastric emptying • Glucose production • e.g.exenatide, liraglutide • Level of GLP1 & GIP • e.g.sitagliptin, vildagliptin
  • 13. 2.AMYLIN ANALOGUE: amylin is secreted from beta cells.(PRAMLINTIDE) 3.DUAL PPAR AGONIST: Aleglitazar, Muraglitazar, Tesaglitazar • Supress glucagon production • Reduce hepatic glucose production • Delay gastric emptying PPAR ALPHA PPAR GAMA (LIVER, VASCULAR WALL) • Inc. circulating HDL • Reduce triglycerides (FAT, MUSCLE) • Modulate glucose metabolism.
  • 14. 4.SGLT2 INHIBITORS: DAPAGLIFLOZIN, CANAGLIFLOZIN,EMPAGLIFLOZIN. • Express in proximal tubule of kidney • Inhibition of glucose reabsorption.
  • 15. INDIA