Key HIV Research From ICAAC 2007: Antiretrovirals in Development and Salvage Chicago, Illinois | September 17-20, 2007 Faculty: Cal Cohen, M.D., M.S. Eric.

Key HIV Research From ICAAC 2007: Antiretrovirals in Development and SalvageKey HIV Research From ICAAC 2007: Antiretrovirals in Development and Salvage

Chicago, Illinois | September 17-20, 2007

Faculty:

Cal Cohen, M.D., M.S.

Eric Daar, M.D.This activity is supported by an educational grant from:

The Body PRO

ICAAC 2007: Antiretrovirals in Development and Salvage

Cal Cohen, M.D., M.S.

Eric Daar, M.D.

Dr. Daar is the chief of HIV medicine at Harbor-UCLA Medical Center in Los Angeles, Calif., and a professor of medicine at the University of California-Los Angeles' David Geffen School of Medicine. He has been an active HIV physician and researcher since the 1980s; during the past three decades, he has led dozens of studies on a vast range of HIV-related issues, with a particular focus on coinfections and other health complications associated

with HIV and HIV treatment, including hepatitis C, metabolic complications, cardiovascular disease and psychosocial issues such as depression.

Dr. Cohen is the research director of the Community Research Initiative of New England and teaches at Harvard Medical School in Boston, Mass. In addition, he works as a HIV clinical management consultant and internist at Harvard Pilgrim Health Care, Boston, Mass., and is affiliated with Harvard Vanguard Medical Associates. Dr. Cohen was co-chair of the Scientific Advisory Committee of amfAR community-based clinical trials network, and served as co-principal investigator of the Harvard/BCH AIDS Clinical Trials Unit, AIDS Clinical Trials Group. He holds appointments at Brigham and Women's Hospital and Beth Israel Hospital, both in Boston, Mass.

Faculty for This ActivityFaculty for This Activity

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ICAAC 2007: Antiretrovirals in Development and SalvageICAAC 2007: Antiretrovirals in Development and Salvage

About this slide presentation

• This presentation is one of three slide sets created to accompany The Body PRO's podcast summary of key research presented at ICAAC 2007, featuring interviews with Cal Cohen, M.D., M.S., and Eric Daar, M.D. To download the remaining slide sets or learn more about this CME/CE program, please visit us on the Web at:

TheBodyPRO.com/ICAAC2007

• Please feel free to use this slide presentation for personal reference or for your own presentations; however, we ask that you not modify any aspects of the slides contained within this presentation, so proper attribution can be retained. If you would like to publish all or part of this presentation, or repost any of these slides online, permission must first be obtained from Body Health Resources Corporation.

• Our gratitude goes out to all who granted permission for their slides to be adapted for this presentation.

DisclaimerKnowledge about HIV changes rapidly. Note the date of this presentation's publication, and before treating patients or employing any therapies described in these materials, verify all information independently. If you are a patient, please consult a doctor or other medical professional before acting on any of the information presented in this presentation.

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Antiretrovirals in Development for Antiretrovirals in Development for Treatment-Experienced PatientsTreatment-Experienced Patients

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Antiretrovirals in Advanced DevelopmentAntiretrovirals in Advanced Development

Drug Name Class Development Stage

Notes

elvitegravir (GS-9137, JTK-303)

Integrase inhibitor

Phase II • Regimens including boosted PIs could have greater antiviral activity.• No clinically relevant drug interaction with etravirine.• When boosted, increases maraviroc exposure.• Showed synergistic interactions with enfuvirtide (T-20, Fuzeon), darunavir (TMC114, Prezista) and efavirenz (Sustiva, Stocrin) in vitro.

etravirine (TMC125)

NNRTI Phase III • No clinically relevant drug interaction with elvitegravir.

maraviroc (Selzentry)

CCR5 inhibitor Phase III • Patients failing regimen had higher mean CD4 increases even with D/M or X4-tropic virus.• Exposure increases when used with boosted elvitegravir; use reduced dose of 150mg twice daily.

raltegravir (MK-0518)

Integrase inhibitor

Phase III • In patients with limited treatment options, all doses had potent and durable effects.

vicriviroc (SCH 417690,

SCH-D)

CCR5 inhibitor Phase II • No adverse effect on white blood cell counts.• Not associated with an increased risk of infections.

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24-week primary analysis

• DUET-1 and -2 differed only in geographical location; pooled analysis was pre-specified

• Plasma viral load >5,000 HIV-1 RNA copies/mL and stable therapy for ≥8 weeks

• ≥1 NNRTI RAM, at screening or in documented historical genotype

• ≥3 primary PI mutations at screening

• Patients recruited from Thailand, Australia, Europe and the Americas

Screening6 weeks

600 patients target per trial

48-week treatment period with optional 48-week extension

*BR = darunavir/ritonavir with optimised NRTIs and optional enfuvirtide

TMC125 + BR*

Placebo + BR*

Follow up4 weeks

DUET: Study Design and Major Inclusion CriteriaDUET: Study Design and Major Inclusion Criteria

BR = background regimen; RAM = resistance-associated mutation

Pedro Cahn et al. ICAAC 2007; abstract H-717. Reprinted with permission.

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DUET: Viral Load Reduction From Baseline (ITT NC=F)DUET: Viral Load Reduction From Baseline (ITT NC=F)

BR = background regimen; SE = standard error; ITT = intent-to-treat population; NC=F = noncompleter equals failure imputation algorithm;

changes below the detection limit (<50 copies/mL) were imputed as 49 copies/mL

–1.7

–2.4

Mea

n c

han

ge

in v

iral

load

fro

m

bas

elin

e (l

og

10 c

op

ies/

mL

) ±

SE

0.0

–0.5

–1.0

–1.5

–2.0

–2.5

–3.0

–3.5

Time (weeks)

0 4 8 12 16 20 24

p<0.0001

TMC125 + BR (n=599)Placebo + BR (n=604)


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DUET: Change in CD4 Cell Count From Baseline (ITT NC=F)DUET: Change in CD4 Cell Count From Baseline (ITT NC=F)

+86

+67

Mea

n c

han

ge

in C

D4

cell

cou

nt

fro

m b

asel

ine

(cel

ls/m

m3 )

± S

E

Time (weeks)

p<0.0001

BR = background regimen; SE = standard error; ITT = intent-to-treat population; NC=F = noncompleter equals failure imputation algorithm

100

75

50

25

00 4 8 12 16 20 24

TMC125 + BR (n=599)Placebo + BR (n=604)


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DUET: Response (<50 copies/mL) According to Enfuvirtide (ENF) Use (Primary Analysis)

DUET: Response (<50 copies/mL) According to Enfuvirtide (ENF) Use (Primary Analysis)

Pat

ien

ts w

ith

vir

al lo

ad

<50

co

pie

s/m

L a

t W

eek

24 (

%)

p<0.0001

Using de novo ENF

DRV FC category, %

TMC125 + BR Placebo + BR

<2 20 27

2–10 40 39

10–40 26 26

>40 15 8

Placebo + BR (n=604)TMC125 + BR (n=599)

67%

Using de novo ENF

p=0.427

34%

56%

Unadjusted response

rates

0

20

40

60

80

Re-using or not using ENF

62%

DRV = darunavir FC = baseline fold change

Using de novo ENF

p<0.05

62%

73%

Adjusted for differences in baseline DRV FC between

groups


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DUET: Response (<50 copies/mL) According to Number of Active Background Antiretrovirals

DUET: Response (<50 copies/mL) According to Number of Active Background Antiretrovirals

0 20 40 60 80 100

2

1

0

Patients with viral load <50 copies/mL at Week 24 (%)

Nu

mb

er o

f fu

lly a

ctiv

e b

ackg

rou

nd

AR

Vs

(PS

S) 45%

60%

8%a

≥

30%

67%74%

Analysis excludes patients who discontinued except for virological failure; PSS = phenotypic sensitivity score; darunavir and enfuvirtide are counted as fully active if FC<10 or used de novo, respectively

7/91

40/88

63/211

120/199

171/257

191/258

Placebo + BR (n=559)TMC125 + BR (n=545)


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DUET: ConclusionsDUET: Conclusions

• In treatment-experienced patients, including those with NNRTI resistant virus, TMC125 consistently demonstrated superiority over placebo– 59% of patients achieved confirmed undetectable VL (<50 copies/mL) with TMC125

plus BR at Week 24

• Even in the absence of any other fully active background agents, with TMC125, 45% of patients achieved undetectable (<50 copies/mL)viral load– response rates increased as more active agents were used in the background regimen

• 13 TMC125 resistance-associated mutations (TMC125 RAMs) were identified– the greatest added benefit in the TMC125 versus placebo group was seen in patients

with <3 TMC125 RAMs– 86% patients had <3 TMC125 RAMs

• Except for rash, incidence and severity of AEs with TMC125 were similar to placebo

• TMC125 has the ability to extend and enhance the NNRTI class and provide a new treatment option for patients with resistance to other NNRTIs


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Protocol 004: Study DesignProtocol 004: Study Design

Interim Analysis of Part I Before Initiating Part IIInterim Analysis of Part I Before Initiating Part II

Raltegravir 600 mg BIDRaltegravir 600 mg BID




Placebo BIDPlacebo BID

Part I cohort: Rx-naive patients stratified and randomized to integrase monotherapy or placebo for 10 days

Part I cohort: Rx-naive patients stratified and randomized to integrase monotherapy or placebo for 10 days

Integrase Monotherapy for 10 Days

Part II cohort: Rx-naive patients stratified and randomized to combination therapy for 48 weeks

Part II cohort: Rx-naive patients stratified and randomized to combination therapy for 48 weeks

~ 30 pts

~ 30 pts

~ 30 pts

~ 30 pts

~ 30 pts

Combination TherapyTotal

~ 38 pts

~ 38 pts

~ 38 pts

~ 38 pts

~ 38 pts

Part I Part II

~ 8 pts

~ 8 pts

~ 8 pts

~ 8 pts

~ 8 pts

Raltegravir 600 mg BID + TDF/3TCRaltegravir 600 mg BID + TDF/3TC




Efavirenz 600 mg QD + TDF/3TCEfavirenz 600 mg QD + TDF/3TC

Adapted from Martin Markowitz et al. IAS 2007; abstract TUAB104.

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Protocol 005: Study DesignProtocol 005: Study Design

Raltegravir 200 mg BID* (43)Raltegravir 200 mg BID* (43)



Placebo BID* (45)Placebo BID* (45)

Raltegravir 400 mg BID* (178)

Raltegravir 400 mg BID* (178)

Weeks 1-24 Weeks 25-48

All 178 HIV-infected participants had anHIV RNA > 5,000 copies/mL and documented

resistance to three classes of oral ARTs at baseline.

*All patients received optimized background therapy.

All 178 HIV-infected participants had anHIV RNA > 5,000 copies/mL and documented

resistance to three classes of oral ARTs at baseline.

*All patients received optimized background therapy.

Adapted from Beatrice Grinsztejn et al. ICAAC 2007; abstract H-713.

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Protocol 005: Patient and Optimized Background Therapy (OBT) Characteristics

Protocol 005: Patient and Optimized Background Therapy (OBT) Characteristics


Raltegravir (MK-0518) + OBT Placebo + OBT

200 mg

N = 43

400 mg

N = 45

600 mg

N = 45 N = 45

Percentage Male

Median Age in Years

Median Years of Prior Antiretrovirals

Mean CD4 Count in mm3

Mean HIV RNA in log10copies/mL

84

43

10

245

4.6

89

43

11

221

4.8

91

44

9

220

4.7

89

43

10

274

4.7

OBT: Median Number of Antiretrovirals

Phenotypic Sensitivity Score*: 0 to Protease Inhibitors

Phenotypic Sensitivity Score*: 0 to All Antiretrovirals

Genotypic Sensitivity Score*: 0 to All Antiretrovirals

Number of Patients With Enfuvirtide (T-20, Fuzeon) as New OBT

4

42 (98%)

20 (47%)

27 (63%)

13 (30%)

4

42 (93%)

26 (58%)

38 (84%)

8 (18%)

4

40 (89%)

22 (49%)

35 (78%)

13 (29%)

4

38 (84%)

18 (40%)

28 (62%)

10 (22%)

*By Phenosense GTNote: Enfuvirtide is not included in the phenotypic sensitivity score since there is no clinical cut-off.

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Protocol 005: Time to Loss of Virologic Response to Week 72: Raltegravir (MK-0518) All Doses Combined vs. Placebo

Protocol 005: Time to Loss of Virologic Response to Week 72: Raltegravir (MK-0518) All Doses Combined vs. Placebo


Placebo

45 11 11 11 9 9 8 6 5 5 4 3 1

133122122 122 120 113 100 95 92 86 69 43 12

02 4 8 12 16 24 32 40 48 56 64 72

Week

0

20

40

60

80

100 %

of

Pat

ien

ts R

emai

nin

g

HIV

RN

A <

400

cop

ies/

mL

# of Patients at Risk

Raltegravir All Doses Combined

Placebo

Raltegravir All Doses Combined*

Placebo*

* Plus optimized background therapy.Patients who never achieved HIV RNA <400 copies/mL were considered failures. Non-responders assigned failure at time 0.

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Protocol 005: Analysis of Raltegravir (MK-0518) ResistanceProtocol 005: Analysis of Raltegravir (MK-0518) Resistance


Study found no association between dose and/or drug concentration and resistance.

The factors decreasing likelihood of developing mutations at amino acids 148 alone, 155 alone, and either 148 or 155 were found to be:

• Phenotypic sensitivity score > 0.

• Lower viral load (≤ 100,000 copies/mL vs. > 100,000 copies/mL).

• New use of enfuvirtide (T-20, Fuzeon) in optimized background therapy.

From: Hazuda et al, XVI International HIV Drug Resistance Workshop, 2007, Barbados

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Protocol 005: Safety During Double-Blind Study PeriodProtocol 005: Safety During Double-Blind Study Period


Raltegravir (MK-0518) safety profile for all doses similar to placebo Liver function test abnormalities were uncommon

• No grade 4 abnormalities for aspartate aminotransferase (AST), alanine transaminase (ALT) or alkaline phosphatase (ALP)

• Grade 3 AST: 2/133 patients (1.5%) in all MK-0518 groups • Grade 3 ALT: 1/133 patients (0.8%) in all MK-0518 groups

Most clinical adverse events (AEs) were mild to moderate 4 serious, drug-related clinical AEs

• Acute pancreatitis after 2 doses, considered 2º to optimized background therapy (200 mg group)

• Metabolic acidosis and renal insufficiency; sepsis; death (600 mg group)• Lacunar infarction by CT (placebo)• Worsening lipoatrophy (placebo)

2 discontinuations due to drug-related AE• Elevated AST/ALT, considered 2º to optimized background therapy (200

mg group)• Lipoatrophy (placebo)

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Elvitegravir (EVG) Phase 2 Study SchemaElvitegravir (EVG) Phase 2 Study Schema

Andrew Zolopa et al. ICAAC 2007; abstract H-714. Reprinted with permission.

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Elvitegravir Study: HIV RNA < 50 copies/mL at Week 16 for Patients With First Use of T-20

Elvitegravir Study: HIV RNA < 50 copies/mL at Week 16 for Patients With First Use of T-20


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Week 16 HIV RNA < 50 copies/mL for Patients Receiving EVG/r 125 mg: Impact of Gradations in Activity of Optimized Background Therapy

Week 16 HIV RNA < 50 copies/mL for Patients Receiving EVG/r 125 mg: Impact of Gradations in Activity of Optimized Background Therapy


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23

44 45

0

1020

30

4050

60

70

8090

100

* versus OBT alone† HIV-1 RNA value imputed as baseline if missing or if patient discontinued before 24 weeks

‡ Last observation carried forward

MOTIVATE 1 and 2: Summary of Week 24 Efficacy ResultsMOTIVATE 1 and 2: Summary of Week 24 Efficacy Results

Includes all patients who received at least one dose of study medication

Mea

n ch

ange

from

ba

selin

e in

CD

4 co

unt (

cells

/mm

3 )MVC QD + OBT (N=414)

MVC BID + OBT (N=426)

OBT alone (N=209)

P<0.0001* P<0.0001*57

109 106

0

20

40

60

80

100

120

Patie

nts

(%)

P<0.001* Difference: +51(95% CI: 33, 69)

P<0.001* Difference: +49(95% CI: 31, 67)

HIV-1 RNA <50 copies/mL†

Mean Change from Baseline in CD4 Count‡

Elna van der Ryst et al. ICAAC 2007; abstract H-715. Reprinted with permission.

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Characterization of Maraviroc Resistance in MOTIVATE 1 and 2: Study Overview

Characterization of Maraviroc Resistance in MOTIVATE 1 and 2: Study Overview

OBJECTIVE: To study changes in HIV-1 tropism in patients who experienced treatment failure in the MOTIVATE 1 and 2 studies

MOTIVATE 1 and MOTIVATE 2 Phase 3 studies in treatment-experienced patients (N=1,075)

Assessment of CD4 count at failure, time of failure, and occurrence of Category C events

by tropism result

NR/NPNon-reportable/

non-phenotypable

D/M*†

Dual/mixed tropic virus population

R5*

Only CCR5-tropic virus detected

X4†

Only CXCR4-tropic virus detected

Tropism determined for all patients at screening, baseline, and all visits where VL>500 c/mL (Trofile™

assay, Monogram Biosciences)

* CCR5-using virus; †CXCR4-using virusElna van der Ryst et al. ICAAC 2007; abstract H-715. Reprinted with permission.

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R5X4A) Pure

B) Mixed

MOTIVATE 1 and 2: Viral Populations That May Exist Within a Patient

MOTIVATE 1 and 2: Viral Populations That May Exist Within a Patient

R

X

XX

X

XX

XXX

XX

XX

XX X

XX

RR

RR

RR R

RRRR R

RR

RRR

RRR

DDDD

DDD D DD

DD

D DD D D D

DD

R

XX X X X XX X X X X

XX X XXXXX

XX

X X X

X XX

X X

X X X

XX

R R RRR R

R R RRRR R

RR

RR R

RR

RR R

R

R

RR

D D

DD

DD


Dual/mixed (D/M) tropism

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-100 0 100 200 300

0

100

200

300

400

500

MOTIVATE 1 and 2: CXCR4-Using Clones Were Detected at Low Frequency in the Baseline Sample

MOTIVATE 1 and 2: CXCR4-Using Clones Were Detected at Low Frequency in the Baseline Sample

Time Since First Administration (Day)

• CXCR4-using clones detected at baseline (7%)

• No CCR5-tropic clones on treatment

R5 R5 DM DM DM DM DM DM R5 R5

1

2

3

4

5

6

HIV

-1 R

NA

(lo

g10

co

pie

s/m

L)

CD

4 C

ou

nt

(ce

lls/m

m3 )

Patient T6

Lewis M et al. XVI International HIV Drug Resistance Workshop, June 2007, Abstract 56 Elna van der Ryst et al. ICAAC 2007; abstract H-715. Reprinted with permission.

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MOTIVATE 1 and 2: Selective Inhibition of R5 Viruses Can Lead to a Change in Tropism Result to D/M or X4


R R RRR R RR

R R RRR R DR

R R RRR R RR

R R RRR R DR

R R RRR R RR

R R RRR R DR

R R RRR R RR

R R RRR R DR

R R RRR R RR

R R RRR R DR

R R RRR R RR

R R RRR R XR

R R RRR R RR

R R RRR R DR

R R RRR R RR

R R RRR R DR

D

X

D

D

D

D

D

D

R5 D/M

Trofile™ (like all resistance tests) measures relative proportions (not absolute amounts) of different viruses (Panel A)

Selective inhibition of a majority virus type, increases the sensitivity to detect the minor variant (Panel B)

A B

MVC


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• Maraviroc selectively inhibits R5 virus

• If maraviroc is administered as part of a sub-optimal regimen, pre-existing low (undetected) levels of D/M or X4 virus will emerge as the dominant viral population

• Since the D/M or X4 virus is pre-existing, time to failure is shorter than with R5 virus (where maraviroc resistance must be selected de novo)

• Similar to the rapid outgrowth of pre-existing (archived) drug-resistant virus when failed ARV therapy is reinitiated after treatment interruption

• After withdrawal of maraviroc, selective pressure on R5 virus is removed, allowing R5 virus to re-emerge as the dominant population

• Reversion to R5 takes approximately 16 weeks, consistent with loss of 3TC1 or enfuvirtide2 resistance after withdrawal of these ARVs

1. Deeks S, et al. J Infect Dis 2005; 192:1537-44.2. Deeks et al. J Infect Dis 2007;195:387-91.


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Randomization 1:2:2

N=601

MOTIVATE 1: Trial DesignMOTIVATE 1: Trial Design

OBT* + maraviroc (150 mg† BID)

OBT* + maraviroc (150 mg† QD)

OBT* + placebo

0 24w

* OBT = optimized background therapy of 3–6 ARVs (PK boosting doses of RTV not counted as an ARV)† Patients receiving a PI (except TPV) and/or delavirdine in their OBT received 150 mg dose of MVC,

all other patients received 300 mg dose of MVC

Screening(6 weeks) 48w

Patients stratified by:• Enfuvirtide use in OBT • HIV-1 RNA < and ≥100,000 copies/mL at screening

Patient eligibility criteria: • R5 HIV-1 infection• HIV-1 RNA ≥5,000 copies/mL

• Stable pre-study ARV regimen, or no ARVs for ≥ 4 weeks• Resistance to and/or ≥ 6 months’ experience with ≥ one ARV from three classes (≥ two for PIs)

Jacob P. Lalezari et al. ICAAC 2007; abstract H-718a. Reprinted with permission.

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MOTIVATE 1 – Week 48:Mean Change From Baseline in HIV-1 RNA

MOTIVATE 1 – Week 48:Mean Change From Baseline in HIV-1 RNA

-1.03-0.80

-1.82-1.66

-1.95-1.82

-2.5

-2.0

-1.5

-1.0

-0.5

0.0

Includes all patients who received at least one dose of study medication

HIV-1 RNA value imputed as baseline if patient discontinued before 48 weeks*Treatment difference vs OBT alone

Mea

n ch

ange

in H

IV-1

RN

A f

rom

bas

elin

e (lo

g 10 c

opie

s/m

L)

Difference: -0.85* (97.5% CI: -1.22, -0.49) Difference: -1.02*

(97.5% CI: -1.39, -0.66)

MVC QD + OBT (N=232)

MVC BID + OBT (N=235)

OBT alone (N=118)

Study week

Difference: -0.79* (97.5% CI: -1.14, -0.44)

Difference: -0.92* (97.5% CI: -1.28, -0.57)

24 48


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MOTIVATE 1 – Week 48:Percentage of Patients With Undetectable HIV-1 RNA

MOTIVATE 1 – Week 48:Percentage of Patients With Undetectable HIV-1 RNA


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Patie

nts

(%)

N=

Maraviroc QD + OBT Maraviroc BID + OBT OBT alone

MOTIVATE 1 and 2: Proportion of Patients Receiving ENF With Undetectable HIV-1 RNA at Week 48 According to ENF First Use

MOTIVATE 1 and 2: Proportion of Patients Receiving ENF With Undetectable HIV-1 RNA at Week 48 According to ENF First Use

<400 copies/mL <50 copies/mL

3

2736

3

25

6471

35 32

61

71

43

0102030405060708090

100

Last observation carried forward

ENF first use ENF experienced/resistance

91 10859 30 75 72

ENF first use ENF experienced/resistance

91 10859 30 75 72


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MOTIVATE 1 and 2 – Week 48: Change in CD4+ Cell Count From Baseline by Tropism Result at Time of Failure

MOTIVATE 1 and 2 – Week 48: Change in CD4+ Cell Count From Baseline by Tropism Result at Time of Failure

Tropism result, Baseline→ Treatment Failure

Mean change from baseline in CD4+ count in patients with treatment failure (cells/mm3 )

OBT aloneN=271

MVC QD + OBTN=477

MVC BID + OBTN=487

All treatment failures* +24 (n=111)

+64 (n=92)

+74 (n=96)

R5→ R5 +25(n=89)

+77(n=33)

+133(n=24)

R5→ D/M or X4 +61(n=6)

+47(n=35)

+57(n=41)

* Includes patients with non-reportable/non-phenotypable tropism result at baseline and patients with non-reportable/non-phenotypable/missing tropism result at time of failure


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ICAAC 2007: Antiretrovirals in Development and SalvageICAAC 2007: Antiretrovirals in Development and Salvage

• Visit The Body PRO for Comprehensive Coverage of ICAAC 2007.This presentation is one of three slide sets created to accompany The Body PRO's podcast summary of key research presented at ICAAC 2007, featuring interviews with Cal Cohen, M.D., M.S., and Eric Daar, M.D. To download the remaining slide sets or learn more about this, please visit us on the Web at: TheBodyPRO.com/ICAAC2007

• In addition, be sure to browse through The Body PRO’s extensive coverage of ICAAC 2007, which includes:– Downloadable MP3s and full transcripts– Expert discussion of key research– Slides and in-depth data analyses

• Visit TheBodyPRO.com/ICAAC2007 today for a full listing of our conference materials!

Key HIV Research From ICAAC 2007: Antiretrovirals in Development and Salvage Chicago, Illinois | September 17-20, 2007 Faculty: Cal Cohen, M.D., M.S. Eric.

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