Evaluation of anti-obesity drugs

Evaluation of Anti-
Obesity Drugs
Dr. Nishtha Khatri
Guide: Dr. Raakhi Tripathi

Flow of seminar
 Introduction
 Pathophysiology
 Current treatment and it’s limitations
 Preclinical evaluation
• In vitro
• In vivo
 Clinical evaluation
 Drugs in the pipeline
 Conclusion

Abnormal or excessive fat accumulation that presents a risk to
health
Multifactorial disorder in which calorie intake over the long
term exceeds energy output
Introduction
Ritter J. Flower R. Hendersen G, Rang H. Rang and Dale's pharmacology. 8th ed. Edinburgh:
Elsevier/Churchill Livingstone; 2015.

WHO- “Epidemic of the 21st century”
Obesity rates
2016- 1.9 billion overweight and 650 million obese individuals1
Obesity prevalence: 2
Women: 13% (2006) to 21% (2016)
Men: 9% (2006) to 19% (2016)
Past 10 years  Doubled
1.WHO fact sheets: Obesity and Overweight. 2017 [Accessed on 28 May 2018]. Available from:
http://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight
2.National Family Health Survey (NFHS-4). 2015-2016 [Accessed on 28 May 2018]. Availble
from: http://rchiips.org/nfhs/NFHS-4Reports/India.pdf

Classification BMI
Underweight < 18.5 kg/m2
Normal weight 18.5 kg/m2 – 24.9 kg/m2
Overweight 25 kg/m2 – 29.9 kg/m2
Obesity (class 1) 30 kg/m2 – 34.9 kg/m2
Obesity (class 2) 35 kg/m2 – 39.9 kg/m2
Extreme obesity (class 3) > 40 kg/m2
Obesity: identification, assessment and management. NICE Guidelines.2014 [Accessed on 26th May, 2018].
Available from: https://www.nice.org.uk/guidance/cg189
Classification of obesity

Obesity-
India
Normal
Overweight
Obesity
18.0-22.9 kg/m2
23.0-24.9 kg/m2
>25 kg/m2
1.WHO Expert Consultation. Appropriate body-mass index for Asian populations and its implications for policy and
intervention strategies. Lancet. 2004 Jan 10;363(9403):157-63. Review. Erratum in: Lancet. 2004 Mar
13;363(9412):902.
2. Misra A, Chowbey P, Makkar BM, Vikram NK, Wasir JS, Chadha D, Joshi SR, Sadikot S, Gupta R, Gulati S, Munjal YP.
Consensus statement for diagnosis of obesity, abdominal obesity and the metabolic syndrome for Asian Indians and
recommendations for physical activity, medical and surgical management. 2009 Feb;57:163-70.

Ritter J. Flower R. Hendersen G, Rang H. Rang and Dale's pharmacology. 8th ed. Edinburgh:
Elsevier/Churchill Livingstone; 2015.
Causes
of
obesity
Dietary
Lifestyle
Genetic
Deficiency in
synthesis or
action of
hormones
Hypothalamic
neuronal system
defect
Defects in
systems
controlling
energy
Drug
induced

Orexigenic Anorectic
Neuropeptide Y (NPY) Corticotropin-Releasing
Hormone
Agoutin-related peptide (AgRP) Melanocyte Stimulating
Hormone
Orexins A and B Cholecystokinin
Galanin Glucagon-like peptide 1
β endorphin Calcitonin gene-related peptide
Norepinephrine Bombesin
Growth Hormone-Releasing
Hormone
Leptin
Melanin concentrating hormone Amylin
Ghrelin PYY
Gupta S. Drug Screening Methods. 3rd ed. The Health Sciences Publisher; 2016.
Role of peptides, hormones and neurotransmitters

Brunton L, Hilal-Dandan R, Knollmann B. Goodman and Gilman's The pharmacological basics
of therapeutics. 13th ed. New York: Mcgraw-Hill; 2018.
Lifestyle modifications
Medical treatment
Surgical treatment

Lifestyle Modifications
Behavioral
modification
Physical exercise
Dietary
modification
Wadden TA, Webb VL, Moran CH, Bailer BA. Lifestyle Modification for Obesity: New Developments
in Diet, Physical Activity, and Behavior Therapy. Circulation. 2012;125(9):1157-1170.

Drug/Drug
combination
Drug group MOA Toxicity
Orlistat GI lipase
inhibitor
Reduces
absorption of
lipids
Decreased absorption
of fat soluble vitamins,
flatulence, fecal
incontinence
Liraglutide GLP-1 agonist Decreases
appetite
Nausea, Vomiting,
pancreatitis
Lorcaserin 5HT2c agonist Decreases
appetite
Headache, nausea,
dry mouth, dizziness,
constipation
Naltrexone/
Bupropion
Opioid
antagonist
+antidepressant
Inhibits
reuptake of
serotonin,
dopamine, NE
Headache, nausea,
dizziness, constipation
Phentermine/
topiramate
Sympathomimet
ic + anti-seizure
Norepinephrine
release in CNS
Insomnia, dizziness,
nausea, paresthesia,

Timeline
1999
2012
2012 2014
2014
Orlistat Phentermine
Topiramate
Liraglutide
Lorcaserin
Naltrexone
Bupropion
Barja-Fernandez S, Leis R, Casanueva FF, Seoane LM. Drug development strategies for the treatment of obesity:
how to ensure efficacy, safety, and sustainable weight loss. Drug design, development and therapy. 2014;8:2391.

Barja-Fernandez S, Leis R, Casanueva FF, Seoane LM. Drug development strategies for the treatment of obesity:
how to ensure efficacy, safety, and sustainable weight loss. Drug design, development and therapy. 2014;8:2391.

Bariatric surgery
O'Brien P. Surgical Treatment of Obesity. [Updated 2016 Jan 19]. In: De Groot LJ, Chrousos G, Dungan K, et al.,
editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK279090/
Indication: BMI > 40 kg/m2 or > 35 kg/m2 with comorbidities
 Roux-en-Y gastric bypass
Vertical-sleeve gastrectomy
 High costs
 Weight regain risk- 5 to 20 % patients

Need for new drugs
 Obesity is associated with major complications and prevalence is
 There are only 5 approved USFDA drugs
 Need for safer compounds with increased efficacy
 All the available medical treatment options reduce weight
modestly by 5.8-8.8 % (1 year) while bariatric surgery can reduce
weight by 16-32 %
 Needs for drugs with multiple targets
 Rogers et al. “The history of anti-obesity drug development is far
from glorious, with transient magic bullets and only a handful of
agents currently licensed for clinical use”

Animal models of
obesity
In Vitro In Vivo
Preclinical evaluation

In Vitro models
1.Determination of plasma leptin
2.Receptor assay for neuropeptide Y
3.Receptor assay of orexin
4.Receptor assay of galanin
5.Adipsin expression in mice
6.β3-adrenoceptor activity
Vogel H. Drug discovery and evaluation. 3rd ed. Berlin: Springer; 2008.

Advantages:
1. A large number of compounds can evaluated in a short period
of time
2. Limited amount of material required
3. Less number of animals required
Disadvantages:
1. Limit discovery of mechanically novel substance
2. Complicated procedures
3. Require technical expertise
4. Costly

Determination of plasma leptin
Principle: Leptin  Circulating
hormone  Maintenance of body
weight  Leptin ↓ in obesity
Method: Radioimmunoassay
Variable: Leptin peptide  Determined
by rat-specific antibody
Modification: Immunoprecipitation 
Precipitation of protein antigen using
an antibody

Receptor assay of neuropeptide Y
Principle: NPY ￪ food intake and ↓ thermogenesis
Method: Specific binding  Difference between the amount of 125 I-
labeled peptide bound in the absence and presence of unlabeled
peptide
Variable: 125I-labeled NPY levels
Modification: Bioassays done for classification of NPY receptors
1. Y1 receptor- Rat kidney, Rabbit saphenous vein
2. Y2 receptor-Rat vas deferens & colon, Dog saphenous vein
3. Y4 receptor-Rat colon
4. Y5 receptor-Rabbit ileum
The Y5 antagonists MK-0557 and S-2367

Receptor assay for orexin
Principle: Orexin A & B bind both to OX1 & OX2
Orexin Appetite stimulating peptide
Variable: % saturably bound reactivity
Methods:
OX1 and OX2 receptors are produced by PCR from fetal and
adult brain cDNA libraries
1. Cell-bound radioactivity is determined by a γ-counter
2. Radioimmunoassay
Orexin antagonists are potential anti obesity drugs

Receptor assay of galanin
Principle: Galanin ￪ food intake, G protein coupled receptors 
GAL1, GAL2, GAL3
Method: GAL1 – Northern blot assay
GAL2- RT PCR
GAL3- 125I galanin radioligand
Variable: Bound/total count calculated  displacement curves
Method used to test galanin receptor antagonists

Adipsin expression in mice
Principle: Adipsin  ASP Lipogenesis
Method: Mouse adipocytes  transfected with adipsin
expression vector
Variable:
Adipsin levels by RIA
Modification – Concentration in human blood secretion using
sandwich ELISA
Drugs that cause weight loss such as ephedrine and caffeine
have been tested

β3-Adrenoceptor
Principle: β3-Adrenoceptors  weight loss in
obese rodents
 Increased thermogenesis in BAT
 Increased lipolysis in WAT
 Independent of food intake
Method: CHO cells  β Adrenoceptors 
transfected with cAMP response element
luciferase plasmids
Variable: Light production measured
β agonists can be tested (weight loss)

In Vivo models
In Vivo
Diet
induced
Hypothalamic
Virus
induced
Genetic
Monogenic Polygenic Transgenic

 Omnivores
 Consume variety of different foods
 Neuro anatomically similar
 Brain areas play a role in control of food intake
 Different neurotransmitters and peptides produce similar
effects on food intake and energy homeostasis
Ideal animal (Rodent)
Vickers SP, Jackson HC, Cheetham SC. The utility of animal models to evaluate novel
anti‐obesity agents. British journal of pharmacology. 2011 Oct 1;164(4):1248-62.

Disadvantages
 Phylogenetically not closely related to humans
 Difference in physiology of rodents and human (rats do not
have a vomit reflex or gall bladder)
 Feeding and housing environment different (20–23°C)
Energy to keep warm
 Complex psychological factors not taken into account

 Construct validity  Cause of disorder mimicked
 Face validity  Characteristics and specific symptoms
mimicked
 Predictive validity  Effects of pharmacological manipulation
identical
Ideal animal model of obesity

Food induced obesity
Divided into 2
groups
Group 1:
Ordinary purina
rodent chow
Group 2:
Purina chow, corn
oil, condensed milk
Principle: Obesity can be induced in rats by offering a diet
containing corn oil and condensed milk
Variables assessed:
Adipose tissue cell size and number
Plasma lipid and glucose levels
Carcass composition and lipid content

Modification: Cafeteria diet- Supermarket foods like cookies,
cheese, milk chocolate, peanut butter
Advantage: There is good face and construct validity
Disadvantage: Functional genomics  at-least one difference
between obese rats and humans
Genes in lipid metabolism tend to downregulate in obese
humans

Food consumption
Principle: Anorectic activity
Method: Manzidol 3 mg/kg i.p. or 10 mg/kg p.o. standard
Treatment continued for 7 days
Variables assessed:
Individual food intakes in grams at specified time
Average food intake and body weight each day
Oral administration results to be confirmed by parenteral route
 To avoid palatability

Modifications:
Frequency, amount & duration of feed
Stimulation for eating by food deprived technique
Automated feeding monitors
Amount of food Hoarded

Acute models of food intake
• Lean rodents
• Re-feeding models vs freely-feeding
• Mice preferred since amount of compound less
• 5HT6 agonists  Rats
• Duration- 1 week
Chronic models of food intake
• Obese rodents
• Duration- 2-3 months
• More representative of humans

Advantages of acute models
 Lesser amount of compound
 Quick
 Information on potency, efficacy, duration of action
 Side effect profile of compound in vivo
 Selection of compound for chronic testing

Disadvantages of acute models
 Baseline food intakes different  Overnight fasting 
stressor
 Insensitive to drugs with delayed onset of action
 Not relevant to all mechanisms of drug action

Advantages of chronic models
 Chronic effect of drugs on the food intake
 Investigate multiple anti-obesity mechanism of drugs
 Drugs with delayed mechanism of action can be tested
 Determine effect on maintenance of body weight
reduction
Disadvantages of chronic models
 Longer duration
 Influence of external factors

Hypothalamic obesity
Hypothalamus: Lateral feeding center
Medial satiety center
Ventromedial lesions:￪ food intake ￪ Body weight in 3-4 months
Hypothalamic
obesity
Surgically-
induced
Chemically-
induced
Monosodium glutamate
Gold Thioglucose

Surgically induced hypothalamic obesity
Principle: Hyperphagia in rats has been reported after
hypothalamic lesions
Methods: Ventromedial hypothalamus Partial lesions induced
sterotaxically
Variables assessed:
Body weight
Brown adipose tissue enzymes
Guanosine diphosphate binding to brown adipose tissue
Modification: Enhanced expression of rat obese (ob) gene in
adipose tissue of ventromedial hypothalamus (VMH) lesioned
rats

Chemically induced hypothalamic obesity
Monosodium glutamate-induced obesity
Principle: Adiposity can be induced in rats by repeated
subcutaneous injections of monosodium-L-glutamate at an early
stage of life
Method: subcutaneous injections monosodium-L-glutamate  5
consecutive days
Variables: Food consumption and weight gain measured at
weekly intervals

Chemically induced hypothalamic obesity
Goldthioglucose induced obesity
Principle: Intraperitoneal or intramuscular injection of
Goldthioglucose  obesity in mice  Fragmentary disruption of
hypothalamic and extra-hypothalamic areas of the brain
Method: Single intraperitoneal injection of Goldthioglucose
Variables: Food intake registered (2 weeks) and body weight (3
months)
Modifications:
Bipiperidyl mustard  Rats
Obesity in mice  Single intracerebral injection with 4-
nitorquinolone-l-oxide

Virus- Induced obesity
Principle: Canine distemper virus  Disruption of
catecholamine pathways  Obesity (8-10 weeks)
Methodology: Virus inoculated in mice intranasally
Variable: Body weight
Adipose cell size and number
Modification: Borna disease virus in rats

Genetic models of obesity
Monogenic rat models Polygenic rat models
Zucker fatty rat WBN/KOB rat
WDF/TA-FA OLETF
JCR: LA Corpulant Obese SHR
Monogenic mice
models
Polygenic mice models
Yellow obese AyA NZO
Obese (OB/OB) BL/6
FAT/FAT KK-Ay
Tubby
Advantage: Helps in Identification of specific genes and their role in
the regulation of energy balance

Monogenic rat models
WBN/KOB rat

Strain of animal Characteristics Drugs that can be
tested
WBN/KOB rat Pancreatitis
Hyperglycemia,
glucosuria, obesity
Primarily for Anti-
diabetic drugs
Otsuka Long Evans
Tokushima fatty rats
(OLEFTF)
Hyperglycemia,
obesity, hyperplastic
pancreatic islets
Beta 3 adrenoceptor
agonist
Obese SHR rat Obesity, hypertension
and hyperlipidemia,
hyperglycemia
Primarily for Anti-
diabetic drugs

Polygenic rat models
Zucker fatty rat

tested
Zucker fatty rat
(fa gene mutation)
Mild glucose
intolerance,
hyperinsulinemia,
insulin resistance,
obesity
5HT 1 receptor agonist
Beta 3 adrenoceptor
agonist
Anti-diabetics
WDF/TA-FA
(fa gene mutation)
Obesity,
hyperinsulinemia,
hyperlipidemia and
hyperphagia
Primarily anti-diabetics
JCR: LA Corpulant
(Overexpression of ob
gene)
Obesity,
hypertriglyceridemia,
hyperinsulinemia

Polygenic mice models
NZO mice
KK-Ay

tested
NZO Obesity, mild
hyperglycemia, insulin
resistance
BL/6
(Autosomal recessive
mutation)
Obesity, hyperphagia,
hyperglycemia,
Elevated insulin
KK-Ay
(Mutation at Ay
gene locus)
Adiposity and diabetes Beta 3 adrenoceptors
Ciglitazone
Mazindole

Monogenic mice models
Yellow obese mice
Tubby mice

tested
Yellow obese AyA
(Mutation at agouti
gene locus
dominant)
Obesity,
hyperglycemia, insulin
resistance
Obese (OB/OB)
(ob gene
overexpression)
Obesity and insulin
resistance
FAT/FAT
(fat gene mutation)
Adult onset obesity,
hyperinsulinemia and
infertility
Tubby
(Autosomal recessive)
Tripartite phenotype
of blindness, deafness
and maturity onset

Transgenic models
 Knockout of uncoupling protein in adipose tissue: Abolition
of BAT thermogenic function
 Knockout of Mcr4 gene in mice: Inhibition of Mcr4 function
leads to obesity
 Targeted deletion of Mcr3 gene: Increased susceptibility to
diet induced obesity
 MCH (Orexigenic) overexpressing transgenic mice

Assays of anti-obesity activity
Hormonal Metabolic activity
GDP-
binding in
brown
adipose
tissue
Uncoupling
protein &
GLUT4 in
brown adipose
tissue
Resting
metabolic rate
Leptin
mRNA in
adipose
tissue

Determination of leptin mRNA in adipose tissue
Principle: Leptin  Circulating hormone  Maintenance of
body weight
Method: RNA extracted from
• Liver
• Intra-capsular brown adipose tissue
• Epididymal white adipose tissue
Northern blot analysis
Variable: Leptin mRNA levels
Modification: Competitive RT-PCR

Uncoupling protein and GLUT4 in brown adipose
tissue
UCP  Family of inner mitochondrial membrane transporters
 Dissipate the proton gradient  Stored energy to heat
Hirschberg V, Fromme T, Klingenspor M. Test Systems to Study the Structure and Function of Uncoupling
Protein 1: A Critical Overview. Frontiers in Endocrinology. 2011;2:63. doi:10.3389/fendo.2011.00063.

Principle: UCP and GLUT4  Thermogenic activity
Method: Northern blot (mRNA) analysis
Western blot (Protein) analysis
Variable: UCP and GLUT4 is measured
Used to study Beta 3 adrenoceptor agonists
Drugs elevating norepinephrine levels
Peroxisome proliferator-activated receptor-γ
Modification:Injection of Neuropeptide Y into rat hypothalamus
 UCP 1 - Brown adipose tissue
 UCP 2 – White adipose tissue
 UCP 3- Muscle
Mukherjee J, Baranwal A, Schade KN. Classification of Therapeutic and Experimental Drugs for
Brown Adipose Tissue Activation: Potential Treatment Strategies for Diabetes and
Obesity. Current diabetes reviews. 2016;12(4):414-428.

GDP-binding in brown adipose tissue
Brown adipose tissue is the major site for non-shivering
thermogenesis in rodents
Binding of nucleotide guanosine diphosphate to uncoupling
protein or thermogenin:
Indicator of thermogenic activity
Variable assessed:
GDP binding from 3H radioactivity

Resting metabolic rate
Principle: Resting metabolic rate  influenced by various drugs in
normal and obese animals
Method: Closed circuit metabolic system  pressure drop
activates the pressure sensor for O2 replacement  Cycle
repeats
Variable: Consumption of O2

Behavioural model
• Increased or decreased motor activity
• Induction of motor behaviour
Interfere with ability of animal to eat

Clinical
evaluation
Phase I Phase II Phase III Phase IV

Phase I
Objective To establish safety, tolerability, pharmacokinetic
and pharmacodynamic data of the drug in
human
To identify no effect and maximally tolerated
doses
Subjects Obese but otherwise healthy
Dosing Escalating doses based on animal models
Variables ECG, Vitals, Laboratory investigations-
Biochemistry, hematology & urinalysis
Cmax, Tmax, t1/2

Primary outcome: Composite safety and tolerability in terms of
Incidence, severity and dose-relationship of adverse events
over a period of 4 weeks
Secondary outcomes:
1. PK as measured by peak plasma concentration at 4 weeks
2. PK as measured by time to maximum concentration at 4
weeks
3. Elimination half-life at 4 weeks to assess relationship to
weight loss

Phase II
Objective To establish safety and preliminary efficacy
Proof of concept
Blinding Double blind
Dosing Range of doses
Variables Change in body weight
Change in waist circumference,
Waist to hip ratio
ECG, Vitals, Laboratory investigations-
1.Guideline on clinical evaluation of medicinal products used in weight management. European medical
agency. 2016 [Accessed on 29 May, 2018]. Available from:
http://www.ema.europa.eu/docs/en_GB/document_library/Scientific_guideline/2016/07/WC500209942.pdf
2.Guidance for Industry Developing Products for Weight Management. FDA.2007 [Accessed on 29 May,
2018]. Available from:
https://www.fda.gov/downloads/Drugs/Guidances/ucm071612.pdf

The primary endpoints should be: (6 months)
• Mean absolute or percent change in body weight between
the active-product and placebo-treated groups
• Proportion of patients in each treatment group who lose
greater than or equal to 5 percent of baseline weight
Secondary endpoints: (6 months)
• Changes in serum lipids
• Fasting plasma glucose
• Blood pressure
• Waist circumference: Circumference of abdomen midway
between the lower limit of the rib cage and the iliac crest
• Waist to hip ratio: Hip circumference measured as the
maximum circumference over the femoral trochanter
• Soft Lean Mass/Mass of Body Fat- Automated analyzer
• Visceral obesity changes: DEXA scan
• Incidence, severity and dose-relationship of adverse
events

Patient inclusion criteria
• 18 Years to 65 Years
• Body Mass Index (BMI) ≥ 30.0 or ≥ 27 (if co-morbidities +)
• and ≤ 40.0 kg/m2
• Patients in whom at least one trial of an appropriate
weight-reducing diet has proven to be insufficient
• Stable body weight (less than 5% self-reported change
within the last 3 months)

Patient exclusion criteria
• History of surgery or use of device in an that attempt to
promote/aid weight loss
• Use of chronic medications/products within 90 days prior to
prior to enrolment that are known to cause weight gain
• History of participation in any weight loss program within 90
days prior to enrolment
• Known history or evidence of a psychiatric disorder that in
the opinion of the investigator would preclude the subject
from participating in the trial

Phase III
Objective Confirm efficacy and determine safety
Blinding Double blind
Dosing Single efficacious dose from phase II
Variables Change in body weight
Change in hip and waist measurements
ECG, Vitals, Laboratory investigations-

Primary efficacy endpoints:
Year 1: The proportion of patients with a reduction from
baseline body weight of 5% or more
Change in body weight (kg) from baseline at year 1 and the
proportion of patients achieving ≥ 10% reduction in body weight
Year 2: Proportion (%) of Patients Maintaining ≥ 5% Weight Loss
Secondary efficacy endpoints: (1 year and 2 years)
• Change in body weight
• waist circumference and waist to hip ratio
• Soft Lean Mass/Mass of Body Fat
• Visceral obesity changes: DEXA scan
• Incidence, severity and dose-relationship of adverse events
• Change in cardiovascular risk factors
• Change in use of concomitant medications for comorbidities
(i.e., hypertension, dyslipidemia)
• Change in Quality of Life measures: WHOQOL-BREF

Safety considerations
Neuropsychiatric safety- Mood assessments with standardized
rating scales (PHQ-9 and GAD-7 scales)
Abuse potential and withdrawal effects
Cardiovascular safety- Blood glucose, lipid levels, Blood
pressure, Heart rate
Valvulopathy and PAH- ECG

Pediatric population
Pharmacokinetics and dose-ranging studies generally should
include patients with age- and sex-matched BMIs greater than
or equal to the 95th percentile
Initial pediatric studies be limited to adolescents (i.e., 12 to 16
year olds)
The primary efficacy parameter - Change in BMI (e.g., the
mean percent change in BMI and the proportion of patients
who lose greater than or equal to 5 percent of baseline BMI).
Validated assessments of neuropsychiatric function.

Post-marketing surveillance
Aim:- Safety
Information on drug interaction
Effect on obesity complications like Diabetes
Phase IV

Mirabegon: Beta 3 receptor agonist1
Adiponectin receptor agonists  improves insulin
sensitivity, lowers body weight and increases energy
expenditure2
Tesofensine: Inhibits dopamine, norepinephrine and
serotonin) presynaptic reuptake3
Drugs in Pipeline
1.Brunton L, Hilal-Dandan R, Knollmann B. Goodman and Gilman's The pharmacological
basics of therapeutics. 13th ed. New York: Mcgraw-Hill; 2018.
2.Turer AT, Scherer PE. Adiponectin: mechanistic insights and clinical implications.
Diabetologia. 2012;55:2319–2326.
3.Martins A, Morgado S, Morgado M. Anti-obesity drugs currently used and new
compounds in clinical development. World J Meta-Anal. 2014;2(4):135-53.

Drugs in Pipeline
Lactoferrin- Reduce visceral body fat and body weight 1
Metformin- Decreases food consumption and induces small
weight losses in diabetic and non diabetics 2
Cetilistat- GI lipase inhibitor 3
1.Zapata RC, Pezeshki A, Singh A, Chelikani PK. 0700 Anti-obesity and antidiabetic properties of
lactoferrin are independent of calorie intake. Journal of Animal Science. 2016 Oct 1;94:335
2.Martins A, Morgado S, Morgado M. Anti-obesity drugs currently used and new compounds in
clinical development. World J Meta-Anal. 2014;2(4):135-53
3.Gras J. Cetilistat for the treatment of obesity. Drugs Today (Barc). 2013 Dec;49(12):755-9.

Summary
 Obesity is a multifactorial disease associated with
comorbidities
 Multi modality approach is ideal for treatment of obesity
 Animal models have provided an invaluable insight into the
pathophysiology of the obesity
 There is a need to develop newer anti-obesity drugs and
researchers can bear the torch of discovery in this field

Evaluation of anti-obesity drugs

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