VIVUS Investor LuncheonVIVUS Investor LuncheonADA 2008 Scientific MeetingADA 2008 Scientific MeetingOBOB--202 Results202 Results

June 10, 2008June 10, 2008San Francisco, CASan Francisco, CA

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Leland WilsonLeland WilsonPresident and CEO, VIVUS Inc.President and CEO, VIVUS Inc.

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NASDAQ: VVUSNASDAQ: VVUS

This presentation contains forward-looking statements about future products, future financial results and other events that have not yet occurred. Investors should be aware that actual results may differ materially from our expressed expectations because of risks and uncertainties about the future. Pharmaceutical development inherently includes significant risks in development, regulatory approval and commercialization of products. There are no guarantees that future results will meet the Company’s expectations. All Vivus products discussed herein have not been approved by the FDA and should only be used by physicians in clinical trials. Except as previously disclosed, no head to head clinical trials with approved therapies have been performed and data provided for approved therapies is from published sources which we believe are reliable. Data for other approved therapies is provided for information only. Please refer to the Company’s filings with the SEC, including its Form 10K-Annual Report and Forms 10Q-Quarterly Reports, which identify these and other risks and uncertainties that may cause actual results or events to differ materially from those presented.

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AgendaAgendaOpening Leland Wilson, CEO

Treatment of Diabetes Nancy Bohannon, M.D.

OB-202 Results Barbara Troupin, M.D. M.B.A.

FDA Diabetes Guidelines David Orloff, M.D.

Expert Panel Timothy Garvey, M.D.

Nancy Bohannon, M.D.

Thomas Najarian, M.D.

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Vivus ManagementVivus Management

Peter Tam– Sr. Vice President Product and Corporate Development

Dr. Wesley Day– Vice President Clinical Development

Dr. Barbara Troupin– Sr. Director Clinical Development

Dr. Charles Bowden– Director Clinical Development

Craig Peterson– Sr. Director Clinical Research

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Panel of ExpertsPanel of Experts

W. Timothy Garvey, M.D.– University of Alabama, Birmingham

Nancy Bohannon, M.D.– St Luke’s Hospital, San Francisco

David G. Orloff, M.D.– Executive Medical Director Medpace, Inc.– Former Director of the Division of Metabolism and

Endocrinology Products at F.D.A

Thomas Najarian, M.D.– Inventor Qnexa

Dr. Nancy Bohannon, FACP, FACEDr. Nancy Bohannon, FACP, FACE

Director of Clinical Research at the Cardiovascular Risk Reduction Program

at St. Luke’s Hospital San Francisco

Treatment of DiabetesTreatment of Diabetes

Can you treat diabetes through weight loss?

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Prevalence of CVD Risk Factors in Prevalence of CVD Risk Factors in Adults: US, 1961Adults: US, 1961--20012001

Reproduced with permission from National Institutes of Health, National Heart, Lung, and Blood Institute. Fact Book Fiscal Year 2005. 2005:52.

50

40

30

20

10

0

Percent o

f Pop

ulation

Year1960 1965 1970 1975 1980 1985 1990 1995

OverweightHypertensionSmokingHigh cholesterol

2000

60

70

2005

10

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Link Between Obesity and Type 2 Link Between Obesity and Type 2 Diabetes: NursesDiabetes: Nurses’’ Health StudyHealth Study

Colditz GA, et al. Ann Intern Med. 1995;122:481-486.

0

20

40

60

80

100

120

< 22 22-22.9

23-23.8

24-24.9

25-26.9

27-28.9

29-30.9

31-32.9

33-34.9

> 35

BMI (kg/m2)

Age

-Adj

uste

d Re

lativ

e Ri

sk

12

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Adipose Tissue Is an Endocrine OrganAdipose Tissue Is an Endocrine Organ

TNF=tumor necrosis factor; PAI-1=plasminogen activator inhibitor-1

Fat is a secretory/endocrine organEmerging View

LiverPancreas

Muscle

Vasculature

Leptin, fatty acids,adiponectin, TNF-α,PAI-1, cytokines

Fat is an inert storage depotTraditional View

Fatty acids Glycerol

Fatty acids Glucose

Kershaw EE, et al. J Clin Endocrinol Metab. 2004;89:2548-2556.

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Relationship Between Relationship Between IntraIntra--abdominal Adiposity and abdominal Adiposity and

Cardiometabolic RiskCardiometabolic Risk

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No Diabetes Type 2 Diabetes

Courtesy of Wilfred Y. Fujimoto, MD.

Extent of Visceral Fat DistributionExtent of Visceral Fat Distributionin Type 2 Diabetesin Type 2 Diabetes

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Each 1Each 1--cm reduction in waist cm reduction in waist circumference reduces the circumference reduces the

risk of cardiovascular disease risk of cardiovascular disease by 2% to 6% in both men by 2% to 6% in both men

and womenand women

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Behavioral interventionsBehavioral interventions

Several studies has shown that diet and physical activity reduced the incidence of Type 2 diabetes.

Example: The Swedish Malmo study showed that diet and exercise for 5 years in men with IGT reduced the incidence of Type 2 diabetes by 50%.

Eriksson et al, Diabetologia 1991; 34: 891-8

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Surgically Induced Weight Loss:Surgically Induced Weight Loss:An effective therapy for diabetesAn effective therapy for diabetes

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Scopinaro et al.: Results 10 years after Scopinaro et al.: Results 10 years after Biliopancreatic diversion (BPD)Biliopancreatic diversion (BPD)

Weight loss 49 kg (135 kg to 86 kg)

Glucose lowered to 89 mg/dl (reduction of 89 mg/dl from 178 mg/dl)

Tricylcerides lowered by 138% to 82 mg/dl from 220 mg/dl

Cholesterol lowered by 109 mg/dl to 113 mg/dl from 222 mg/dl

Scopinaro et al. Diabetes Care, 28:10, October 2005

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Adjustable Gastric Banding and Adjustable Gastric Banding and Conventional Therapy for Type 2 Conventional Therapy for Type 2 DiabeticsDiabetics

Study: 60 patients, unblinded, randomized controlled trial to determine if surgically induced weight loss results in better glycemic control than conventional approaches

Study period: 2 years

Baseline:Study Conventional

– Weight (kg) 105 105– HbA1c 7.8 % 7.6%– TG (mg/dl) 190 189– SBP (mm Hg) 136 135– DBP (mm Hg) 87 86

Dixon, J. B. et al. JAMA 2008;299:316-323

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Adjustable Gastric Banding and Adjustable Gastric Banding and Conventional Therapy for Type 2 Conventional Therapy for Type 2 Diabetics: ResultsDiabetics: Results

Net Change from Baseline:Study Conventional

– Weight (kg) -21 -1.5– Weight (%) -20.7% -1.7%– HbA1c -1.8 % -0.4%– TG (mg/dl) -72 -2

Remission of type 2 diabetesStudy Conventional

– Patients 73% 13%

Remission was related to weight loss and lower baseline HbA1c

Dixon, J. B. et al. JAMA 2008;299:316-323

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SummarySummary

Obesity directly related to type 2 diabetes

Behavior modifications are helpful but often difficult for patients to achieve and maintain

Surgically induced weight loss of 20% can lead to remission of diabetes

Role of pharmacotherapy induced weight loss in type 2 diabetes….awaiting results.

Effect of Qnexa (phentermine and Effect of Qnexa (phentermine and topiramate) in Type 2 Diabetestopiramate) in Type 2 Diabetes

VIVUS Study OBVIVUS Study OB--202202

WT Garvey , B Troupin‡, P Tam‡, T Najarian‡,

C Peterson‡, WW Day‡

ADA 2008 – San Francisco*University of Alabama, Birmingham

‡ VIVUS, Inc. Mountain View, CA

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OBOB--202 Background:202 Background:Obesity and Cardiovascular Disease SpectrumObesity and Cardiovascular Disease Spectrum

Increased Weight

Insulin Resistance

Cardiovascular Morbidity & Mortality

DiabetesDyslipidemiaHypertension Vascular Inflammation

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The The ““OptimalOptimal”” Diabetes TherapyDiabetes Therapy

Achieves and maintains glucose lowering to guidelines– ADA < 7.0 %, IDF/WHO < 6.5%

Has a beneficial effect on other related comorbidities and ultimately cardiovascular mortality– Weight loss– Lipids– Blood pressure– Inflammation

Well tolerated and convenient (oral)

Demonstrated long term safety for chronic use

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OBOB--202 Background: Qnexa202 Background: Qnexa

Proprietary, low dose, oral combination of two FDA approved drugs

– Phentermine, 15 mg

– Topiramate, 100 mg

Synergistic efficacy in weight loss*

* Gadde K et al, NAASO abstract 55-OR (2006); Najarian T ADA abstract 2733-PO (2007)

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OBOB--202: Study Objective and Endpoints202: Study Objective and Endpoints

Primary: – Glycemic control (HbA1c at week 28)

Secondary: – Fasting Glucose – Blood Pressure– Lipids– Weight loss– Waist circumference

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Placebo (N=104)

Qnexa (N=102)

Screening(2 weeks)

Titration(4 Weeks)

Treatment (24 weeks)

Week -2 Week 0 2 4 8 16 2012 24 28

OBOB--202: Study Design202: Study Design

N=206(10 Centers)

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OBOB--202: Study Inclusion Criteria202: Study Inclusion Criteria

Subjects with type 2 diabetes

Inadequately treated with diet and exercise, oral diabetes medication

18-70 years

HbA1c 7-12%

BMI = 27-45 kg/m²

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OBOB--202: Study Exclusion Criteria202: Study Exclusion Criteria

Use of insulin or incretins

Blood pressure greater than 150/95; triglycerides > 400 mg/dL

History of nephrolithiasis, glaucoma

Inadequately controlled depression

Unstable cardiac, pulmonary, renal, or hepatic disease

Previous bariatric surgery

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OBOB--202: Baseline Demographics202: Baseline Demographics

PlaceboN=104

QnexaN=102

Female (%) 62 75

Mean Age (years) 48.5 50.2

Hispanic/Latino 50% 64%

Black/African American 12% 10%

Weight (kg) 98.1 94.7

BMI (kg/m2) 35.1 35.3

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OBOB--202: Study Population202: Study Population

At study entry– Wide range of duration and severity of

disease– On a variety of oral diabetes medications

During study– Intervention with oral diabetes medications

permitted at any time during treatment

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OBOB--202202: : Baseline Medical HistoryBaseline Medical History

PlaceboN=104

QnexaN=102

Cardiovascular 71% 65%

Central Nervous System 46% 53%

Metabolic (ex-DM2) 48% 50%

Gastrointestinal 57% 56%

Psychiatric 14% 18%

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OBOB--202: Baseline Diabetes Therapy202: Baseline Diabetes Therapy

0

10

20

30

40

50

60

70

Per

cent

age

of S

ubje

cts

Placebo

Qnexa

Drug Naive

Metformin Monotherapy

>2 Diabetes Medications

More than 60% of subjects were on 2 or more diabetes medications

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OBOB--202 Baseline Characteristics: 202 Baseline Characteristics: Time Since Diagnosis of DiabetesTime Since Diagnosis of Diabetes

05

1015202530354045

< 1 year 1-5 yrs 5-10 yrs > 10 yrs

Perc

ent o

f Sub

ject

s

PlaceboQnexa

Approximately 60% of subjects had diabetes for more than 5 years

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OBOB--202: Demographics202: Demographics

Hispanic subjects in Qnexa group represented a majority compared to placebo (p=0.050)

62% of Qnexa subjects were on 2 or more oral diabetes medications– Most subjects were on medication at baseline for

other co-morbidities

60% had diabetes diagnosis greater than 5 years– 30% of Qnexa subjects had diabetes > 10 years

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OBOB--202: Baseline Glycemic Parameters202: Baseline Glycemic ParametersPlacebo

N=104

Qnexa

N=102

Fasting Glucose (mg/dL) 174.0 174.7

Mean HbA1c 8.6% 8.7%

HbA1c 7-8 (% subjects) 38% 39%

HbA1c >8-12 (% subjects) 62% 61%

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OBOB--202 Results: Change from 202 Results: Change from Baseline HbA1c (ITT, LOCF)Baseline HbA1c (ITT, LOCF)

p <0.001 at each time point

-1.4

-1.2

-1

-0.8

-0.6

-0.4

-0.2

0

Baseline Week 16 Week 28

Cha

nge

in H

bA1c

PlaceboQnexa

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OBOB--202 Results: Change in Fasting 202 Results: Change in Fasting Glucose (ITT, LOCF)Glucose (ITT, LOCF)

135

145

155

165

175

Baseline Week 4 Week 16 Week 28

Fast

ing

Glu

cose

(mg/

dL)

QnexaPlacebo

p <0.001 at each time point

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OBOB--202 Results: Change in Diabetic 202 Results: Change in Diabetic Medication During StudyMedication During Study

-20

-10

0

10

20

30

Net

cha

nge*

in M

eds

PlaceboQnexa

* Net change = number of medication additions (or dosage increases) minus number of medication subtractions (or dosage

Number of Meds Dosage of Meds

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OBOB--202 Results:202 Results: % of Subjects Achieving % of Subjects Achieving ADA Glycemic GoalsADA Glycemic Goals

0%

10%

20%

30%

40%

HbA1c < 7.0% HbA1c < 6.5%*

Perc

ent o

f Tre

atm

ent G

roup Placebo

Qnexa

**

Baseline HbA1c: Placebo 8.6%, Qnexa 8.7%

*Incidence of hypoglycemia for Active and Placebo: 6% vs. 5% **p<0.01

**

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OBOB--202 Results: Percent Change in 202 Results: Percent Change in Body Weight (ITT, LOCF)Body Weight (ITT, LOCF)

-10

-8

-6

-4

-2

0

0 2 4 8 12 16 20 24 28

Cha

nge

from

Bas

elin

e (%

Wei

ght L

oss)

QnexaPlacebo

p <0.0001 at each time point

-1.2%

-8.0%

Weeks

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OBOB--202 Results: Changes in CV 202 Results: Changes in CV Risk FactorsRisk Factors

Placebo Qnexa p-value

Systolic Blood Pressure (mmHg) ↑ ↓ <0.01

Diastolic Blood Pressure (mmHg) ↑ ↓ <0.05

Triglycerides (mg/dL) ↑ ↓ ↓ <0.05

Total chol/HDL ↑ ↔ <0.05

Waist Circumference (cm) ↓ ↓ ↓ <0.0001

Patients at study entry were well managed for lipids and BP

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OBOB--202 Results: Adverse Events 202 Results: Adverse Events (% subjects)(% subjects)

Placebo Qnexa

Nausea 5% 18%

Paresthesia 0% 17%

Constipation 2% 10%

Insomnia 4% 9%

Dry Mouth 1% 8%

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OBOB--202 Cognitive Adverse Events202 Cognitive Adverse Events

Cognitive events related to memory and attention, were mild to moderate, and manageable (7 Qnexa, 1 Placebo)

No discontinuations due to cognitive events

6 of 7 Qnexa subjects with cognitive events completed study

Note: Bray reported 23% of subjects had difficulty with memory and 9% had attention/concentration difficulty on the 96 mg topiramate alone dose in a 6 mo weight loss study.

Bray et al, Obesity Research 11:6 (2003)

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OBOB--202 Results: Depression/Mood 202 Results: Depression/Mood ObservationsObservations

Depression/Mood cases were mostly mild, brief and manageable (5 Qnexa, 1 placebo)

3 cases were considered related, 3 unrelated

All Qnexa subjects completed the trial on treatment

No discontinuations due to depression/mood for Qnexa

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OBOB--202: Patient Health 202: Patient Health Questionnaire (PHQQuestionnaire (PHQ--9)9)

PHQ-9: a validated, nine-item tool used to screen for depression at baseline and during the study

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OBOB--202: Mean PHQ202: Mean PHQ--9 Scores (9 Scores (±±SE)SE)

Baseline Week 28

Placebo 2.8 (± 0.24 ) 2.1 (± 0.25 )

Qnexa 3.0 (± 0.31 ) 1.6 (± 0.29 )*

*P<0.05 vs. baseline

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OBOB--202 Results: Retention and 202 Results: Retention and TolerabilityTolerability

Placebo Qnexa

Study Completion 72% 85%

Discontinuation due to AEs 4% 3%

Note: Bray reported 23% dropouts due to AEs for the 96 mg topiramate alone dose in a 6 mo weight loss study.

Bray et al, Obesity Research 11:6 (2003)

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OBOB--202 Results: Safety Summary202 Results: Safety Summary

Discontinuations due to AEs – 3 in Qnexa: colon ca, nausea/vomiting, intermittent

disorientation– 4 in Placebo: colon ca, viral infection, eye

pain/vision change, dry mouth/forgetfulness

No drug related SAEs

Total SAEs– 5 in Qnexa: colon ca, anemia, gallbladder, viral

infection, osteoarthritis– 6 in Placebo: colon ca, cardiac (3), stroke, non-

cardiac chest pain

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0

2

4

6

8

10

12

14

Physicalfunction

Self esteem Publicdistress

Total score

Domains

Cha

nge

from

Bas

elin

e in

QoL

Placebo

Qnexa

*

**

*

* p< 0.05** p< 0.01

OBOB--202: Impact of Weight Loss on 202: Impact of Weight Loss on Quality of LifeQuality of Life

*

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OB 202: Patient SatisfactionOB 202: Patient Satisfaction

“How has the study treatment affected your ability to lose weight and maintain weight loss?”

"Greatly Improved"

0%

10%

20%

30%

40%

50%

60%

70%

Treatment Groups

% o

f Sub

ject

s R

epor

ting

PlaceboQnexa

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OBOB--202 Results: Efficacy Summary202 Results: Efficacy Summary

1.2% reduction in HbA1c from baseline (ITT)

8.0% reduction in weight from baseline (ITT)

Significant improvements seen in:• Systolic and diastolic blood pressure• Triglycerides• Waist circumference• Quality of life (IWQoL)

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VIVUS OBVIVUS OB--202: Conclusion202: Conclusion

Qnexa provided HbA1c reductions comparable to currently available oral diabetic medications, with the additional benefit of significant weight loss and importantly, significant improvement in cardiovascular risk factors

Qnexa was well tolerated

Dr. David OrloffDr. David Orloff

Executive Director of Medical and Regulatory Affairs, Medpace

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U.S. RegulatoryU.S. RegulatoryPerspective on Diabetes Drug Perspective on Diabetes Drug DevelopmentDevelopment

David G. Orloff M.D.Executive Director, Regulatory Affairs

Medpace, Inc.

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FDAFDA’’s guiding principles of drug s guiding principles of drug regulationregulation

Clinical risk vs. benefit calculus

Upside: public health value

Downside: public health risk dictates required level of assurance of safety

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FDAFDA’’s benefits benefit--risk Equation: chronic risk Equation: chronic preventive therapiespreventive therapies

Risk of condition (thus potential benefit of therapy)– Continuum from mild morbidity to mortality– Short-term vs. long-term disease natural history

Benefit of drug:– Meaningful benefits experienced by small or large fraction of treated

patientsDrug tolerability/compliance also factors

– Ancillary “beneficial’ effects– Evidence of risk reduction (biomarkers vs. endpoints)

Risk of drug:– Reversible vs. irreversible– Severity, frequency– Temporal relationship to start of tx, dosing– Monitorability– Manageability: predictability, preventability

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FDA value judgment for a new FDA value judgment for a new drug: public health needdrug: public health need

Risk-benefit evaluations are made in the context of the current armamentarium

Does a new drug address an unmet need?

Does it represent a therapeutic advance?

Can we meet or exceed the effects of the new drug with single or combination approved txs?

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Height of Height of ““barbar”” varies directly with varies directly with size of target populationsize of target population

Expanding the indication increases number potentially to harm, requiring…

Greater assurance of safety, requiring…

Larger numbers of patients studied,

Longer periods of follow up, and

More intensive on-study monitoring

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Risk Management issues for FDARisk Management issues for FDARisk mitigation can never be 100%

– Acceptability of risk relies on nature of risk, both relative and absolute risks, and significance of benefits

– Can entry into the market be moderated?

Can individuals at risk be prospectively identified?

Is monitoring for emergent adverse effects available to permit pre-emptive action?

If adverse effects do arise, are they reversible?

What is the scope of the risk management problem?

Are there built-in risk mitigators (tolerability, route of administration, cost)?

Is it possible to educate around risks?

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Treatment of Diabetes with Obesity Treatment of Diabetes with Obesity Drugs Drugs

2008: a path but no precedents

Standard of evidence of benefit

Safety exposures

Presumptions about labeling

Necessary studies

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Obesity Drugs for DiabetesObesity Drugs for Diabetes

2008: the door has been opened– Weight loss independent effects no longer

needed

Surrogate-based approval: HbA1c– Additionally: reduction in insulin

requirements, reduction in OADs– Need for M&M outcomes conditional on

safety concerns

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Open door: Weight loss with Open door: Weight loss with improvement in glycemia is enoughimprovement in glycemia is enough

No precedents dictating specific clinical development path– Diabetes guidance recommends 2500 total,

1500 for one yr, 500 for 18 months– Presume build on obesity program for safety

FDA may be concerned about overall increased medical risk in DM population compared to non-diabetic obese

Presume MOA-driven CDP

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Diabetes indications now Diabetes indications now ““standardizedstandardized”” with disclaimers as with disclaimers as applicableapplicable

[drug] is indicated as an adjunct to diet and exercise to improve glycemic control in [adults/children] with type 2 diabetes mellitus– Limitations on use: [drug] has not been

studied [as monotherapy or] in combination with [approved agent] nor studied extensively with [approved agent]

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Standard diabetes programStandard diabetes program

Monotherapy: 6-month placebo controlled in naïve/washout patients

Add-on to max or near max doses of one or more OADs (met, SU, TZD, DPP-4i)– FDA believes this mimics SOC– FDA believes avoid issues related to

upward dose titration of background OADs

Add-on to insulin

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Rationale for Unique Development Rationale for Unique Development ProgramProgram

Primary/dominant effect may weight loss-associated improvements in mediators of risk/risk factors

No tendency to directly cause hypoglycemia

Addresses critical/universal management issue in T2DM

Primary PD effect is monitorable, as are multiple secondary risk factor modifications

No clinical reason to “stage” intervention with weight loss agent

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Opportunities in Prevention with Opportunities in Prevention with Effective Weight Loss and Effective Weight Loss and MaintenanceMaintenance

Cardiovascular: hypertension, Cardiovascular: hypertension, coronary artery disease, angina coronary artery disease, angina pectoris, congestive heart failurepectoris, congestive heart failure

Cerebrovascular: strokeCerebrovascular: stroke

HyperlipidemiaHyperlipidemia

Metabolic syndrome/type 2 DMMetabolic syndrome/type 2 DM

CholelithiasisCholelithiasis

Gout, uric acid nephrolithiasisGout, uric acid nephrolithiasis

OsteoarthritisOsteoarthritisObstructive sleep apnea, Obstructive sleep apnea, hypoventilationhypoventilationHyperandrogenism, hirsutism, Hyperandrogenism, hirsutism, irregular menses, complications irregular menses, complications of pregnancy, stress of pregnancy, stress incontinenceincontinenceMalignancies: breast, Malignancies: breast, endometrium, colon, prostateendometrium, colon, prostateIncreased surgical riskIncreased surgical riskPsychological disordersPsychological disorders

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FDAFDA’’s Role in Diabetess Role in Diabetes--Obesity Obesity Drug DevelopmentDrug Development

The magnitude of the obesity epidemic, its contribution to chronic disease, its costs to individuals and society, and the absence of broadly effective therapeutics constitute a “call to action” by the collective medical community, including FDATo advance the field of diabetes-obesity therapeutics, FDA must provide guidance around resolution of issues related to real or perceived barriers to development The “quality” of the diabetes-obesity armamentarium ultimately should be on par with those in other areas of preventive medicine

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Proposed Development PlanProposed Development Plan

Assume that trial scope, design, choice of background tx not fixed– Consider monotherapy vs. placebo in naives or

patients washed out of meds or combination with met as initial tx

– Consider add on to stable regimens “based” on commonly used medication classes

E.g., Metformin-based, TZD alone or in combo, insulin-based, incretin-based

– Consider small study in Type ½– Explore diabetes prevention in IGT

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Leland WilsonLeland WilsonPresident and CEO, VIVUS Inc.President and CEO, VIVUS Inc.

73

Qnexa News Flow 2008Qnexa News Flow 2008

OB-202 ADA presentation Q2 2008

Top-line data from EQUATE (obesity) Q4 2008

Top-line data from DM-230 (diabetes) Q4 2008

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Panel of ExpertsPanel of Experts

W. Timothy Garvey, M.D.,– University of Alabama, Birmingham

Nancy Bohannon, M.D.– St Luke’s Hospital, San Francisco

David G. Orloff, M.D.– Executive Medical Director Medpace, Inc.– Former Director of the Division of Metabolism and

Endocrinology Products at F.D.A

Thomas Najarian, M.D.– Inventor Qnexa

Questions and DiscussionsQuestions and Discussions

VIVUS Investor LuncheonVIVUS Investor LuncheonADA 2008 Scientific MeetingADA 2008 Scientific MeetingOBOB--202 Results202 Results

June 10, 2008June 10, 2008San Francisco, CASan Francisco, CA