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Investigational Therapies for HIV and/or Other Viral Diseases

Dosing Usually 500 mg bid with didanosine
Adverse Effects Bone marrow suppression, sometimes severe and rarely fatal; stomatitis, sometimes severe; rash; hair loss; may increase the risk of ddI-induced pancreatitis and/or peripheral neuropathy especially with concomitant d4T
Interactions Increased neuropathic effect of other neuropathic drugs
Suggested laboratory evaluations Monitor CBC closely at least initially, particularly in the setting of advanced disease
Warnings Bone marrow suppression, sometimes severe and rarely fatal may develop.
Toxicity is unacceptable except for deepest salvage therapy.
Comment By inhibiting ribonucleotide reductase this drug inhibits the cellular formation of deoxynucleoside triphosphates (dNTPs) especially purines which may increase the uptake of antiviral nucleosides by HIV, especially didanosine (ddI) and stavudine (d4T.) It also increases phosphorylation of NRTIs by inducing cellular kinases. The use of hydroxyurea should be considered investigational (8/2002) and possibly hazardous, but it may be considered for salvage therapies where the possible benefits of therapy outweigh the possible risks.  The use of hydroxyurea has not shown consistent clinical benefit despite in vitro and theoretical activity.


Immunomodulator Therapies
interleukin-2 (IL-2)
Expensive ($500/dose x 10 doses/cycle x 3-4 cycles per year), parenteral, and potentially toxic cytokine therapy which reliably raises CD4-counts in persons on fully-suppressive HAART: the clinical significance of these laboratory observations is under investigation.
therapeutic vaccination
[Remune and others]
Under investigation; minimal laboratory indicators of improved immunity are being evaluated for clinical significance
interferon Expensive, parenteral, and toxic therapy of unproven benefit: recent studies indicate interferon may have moderate activity against HIV at 5 million units injected SQ daily. Interferon therapy is approved and useful for Kaposi’s sarcoma and HCV.  It may also be useful against severe HPV.


Other Investigational Therapies
Antiretroviral Therapy for HIV Infection



 Status, Adverse Effects, & Other Information
Capavirine NNRTI May be able to overcome resistance (K103N) to prior NNRTI therapy.  Recent studies show day 15 median (mean) HIV-1 load decreased by 1.34 (1.45) log(10) copies/mL in patients receiving 25 mg/kg/day.4

Capravirine, a new nonnucleoside reverse transcriptase inhibitor (NNRTI), failed to control HIV better than placebo in a 48-week study of people with resistance to NNRTIs, according to a report at the 12th Conference on Retroviruses and Opportunistic Infections held in Boston, Massachusetts. However, a subgroup analysis suggested that a regimen including capravirine, nelfinavir, and two nucleoside reverse transcriptase inhibitors (NRTIs) had some activity against virus resistant to both zidovudine and lamivudine.

In vitro studies indicate that capravirine is able to inhibit some HIV strains resistant to current NNRTIs. Laboratory work also suggests that resistance to capravirine evolves more slowly than to other NNRTIs, Rick Pesano, MD, PhD reported.

The current trial randomized people taking a failing NNRTI regimen to receive 700 mg or 1400 mg of capravirine twice daily or placebo. All participants also received twice-daily nelfinavir and two NRTIs picked on the basis of treatment history and genotype. None of the 179 study participants had been previously treated with a protease inhibitor.

Trial enrollees had moderately advanced disease, with an average viral load around 4.4 log copies/mL and median CD4 counts of 206 cells/mm3 in the placebo group, 248 cells/mm3 in the 700-mg capravirine group, and 249 cells/mm3 in the 1400-mg capravirine group. Resistance to NRTIs and NNRTIs was similar across the study arms.

Pesano reported 48-week failure rates—defined as failure to reduce the viral load by 0.5 log by Week 4, or rebounding after a 0.5 log reduction—of 24% with placebo, 15% with 700 mg of capravirine, and 13% with 1400 mg, differences that were not statistically significant. The reductions in viral load from baseline to Week 48 also did not differ significantly: 2.1 logs, 2.3 logs, and 2.4 logs, respectively.

A 48-week noncompleter-equals-failure analysis determined that 58% of patients taking 1400 mg of capravirine twice daily had a viral load below 400 copies/mL, compared with 43% taking 700 mg twice daily, and 46% taking placebo. These differences also fell short of statistical significance.

In a preplanned analysis of nonrandomized subgroups who began treatment with virus resistant to zidovudine and lamivudine, 54% in the 1400-mg group had a viral load under 400 copies/mL at Week 48, compared with 36% taking 700 mg, and 31% taking placebo. This trend was not statistically significant, however.

The better noncompleter response with 1400 mg of capravirine partly reflects the high dropout rates in the other 2 arms—44% with placebo, 42% with 700 mg capravirine, and 30% with 1400 mg capravirine. Whereas 15% of patients stopped the 700-mg dose because of side effects, 7% stopped the 1400-mg dose for that reason.

Diarrhea affected 65% in the 1400-mg group and 53% in the 700-mg group. However, diarrhea also was reported by 49% given placebo, and the incidence of diarrhea in all treatment arms may have been due to nelfinavir therapy. Rates of nausea were 35% with 1400 mg, 27% with 700 mg, and 20% with placebo.

Dr. Pesano noted that the high failure rates in all three study arms came as a surprise, since people started nelfinavir with no protease inhibitor experience and also began carefully chosen NRTIs. The study outcomes will be further scrutinized as the development of capravirine continues. [CROI 2005:]

PA-457 Maturation
In an initial study, single dose PA-457 was given to 24 men with HIV who were either drug-naive or who had not taken highly active antiretroviral therapy (HAART) for at least 4 weeks. Six men each were given 75, 150, or 220 mg of the drug, or a placebo.  The 150-mg and 250-mg doses cut the median viral load roughly 3-fold (by 0.45 and 0.51 log10 copies/mL, respectively). This is a respectable amount for a single dose of drug. Presenter David Martin compared this with the drugs tenofovir and D-d4FC which in single-dose studies produced median viral load reductions of 0.33 and 0.45 log10 copies/mL, respectively.  The most interesting finding was that the viral reduction appeared to be sustained for many days. PA-457 has a half-life of 2 to 3 days, and a viral load reduction of more than 0.35 log10 copies/mL was maintained for 8 to 9 days after treatment with the 2 larger doses.  Martin announced that a 10-day study of PA-457 monotherapy is ongoing, and phase 2 efficacy studies are planned to start toward the end of 2005. [CROI 2005:]

The Phase II study met its primary endpoint by demonstrating a statistically significant reduction in the level of HIV in the blood compared to placebo.  The median reduction in HIV viral load in the trial was greater than 1 log10, or a 90% decrease, at the highest dose.  The US Food and Drug Administration (FDA) has granted Fast Track designation to PA-457. 

In this randomized double-blind Phase 2a study, performed at leading academic centers in the US, PA-457 at one of four doses (25, 50, 100 or 200mg; 6 patients per group) or placebo (8 patients), was administered orally once daily for 10 days to HIV-infected subjects not on other antiretroviral therapy. The primary endpoint was viral load reduction on day 11.  Other endpoints included safety, tolerability and pharmacokinetics of the drug.

At the 100 and 200 mg doses, PA-457 treatment for 10 days resulted in statistically significant reductions in viral load compared to placebo, with individual decreases of up to 1.7 log10. 

At the 200mg dose level, the median viral load change at Day 11 was -1.03 log10.  Median Day 11 values at the other dose levels were: Placebo:  +0.03 log10; 25mg: +0.05 log10; 50mg: -0.17 log10; 100mg: -0.48 log10.  In patients with baseline viral loads under 100,000 copies/ml the median Day 11 reduction was  -1.52 log10 at the 200mg dose level (three of six patients) and -0.56 log10 at the 100mg dose level (five of six patients).

Genetic analysis of HIV in patients pre- and post- treatment, available now for 21 out of 33 patients in the study, showed no evidence of the development of resistance to PA-457, the same result as seen previously in a single dose study with PA-457. 

All doses were observed to be generally safe and well tolerated with no Grade 3 or 4 laboratory abnormalities. All adverse experiences were mild or moderate and no dose-limiting toxicity was identified.

DPC 681 PI Active against PI-resistant HIV
DPC 684 PI Active against PI-resistant HIV
TMC114/r PI Active against multidrug resistant HIV. 
After 24 weeks of treatment in triple-class-experienced HIV-infected patients, the investigational protease inhibitor (PI) TMC114 controlled resistant HIV significantly better than comparison regimens.[1] Richard Haubrich, MD, from the University of California, San Diego, reported an average viral load drop of 1.85 log copies/mL with the highest dose of TMC114 vs 0.27 log with alternative PI regimens. The findings presented by Dr. Haubrich at the 12th Conference on Retroviruses and Opportunistic Infections in Boston, Massachusetts, raised expectations that ritonavir-boosted TMC114 may be a potent option for people with multiclass resistance. At the highest dose of TMC114/ritonavir, viral loads dropped below 50 copies/mL, even in 5 of 13 people for whom resistance testing could identify no other active antiretrovirals. Researchers from 14 countries tested TMC114/ritonavir at 4 doses—400/100 mg and 800/100 mg once daily, and 400/100 mg and 600/100 mg twice daily—in 397 people with triple-class experience, 1 or more primary PI mutations, an average viral load of 4.61 log10 copies/mL, and an average CD4+ cell count of 136 cells/mm3. Baseline numbers were equivalent in a control group of 100 people randomized to start 1 or 2 alternative boosted PIs selected by their clinicians. Viral load declines at Week 24 averaged 1.85 logs with the highest dose of TMC114 vs 0.27 logs in the control arm in a noncompleter-equals-failure analysis (P < .0001). Mean viral load ebbs in the other TMC114 arms ranged from 1.34 to 1.47 logs. The highest-dose group gained an average 75 cells/mm3, compared with 15 cells/mm3 in the control group. Among people taking the highest dose of TMC114, 47% had a viral load under 50 copies/mL at Week 24 and 72% had at least a 10-fold drop in viral load. Of 40 people in the highest-dose group who had 3 or more primary protease mutations when they started the new PI, 19 had a viralload under 50 copies/mL 24 weeks later. Four of 397 people had to stop TMC114 because of side effects. Overall toxicity rates did not differ significantly between the combined TMC114 groups and the control group. Phase 3 studies using the 600/100-mg twice-daily dose of TMC114/ritonavir are slated to start later in 2005. [CROI 2005:]
TMC1252 NNRTI Possible activity against NNRTI-resistant HIV.  Single mutations which account for <2% of NNRTI mutations (Y181I, Y181V, F227C and M230L) impose <10 fold increase in resistance in 4/59 isolates tested.

The non-nucleoside reverse transcriptase inhibitor (NNRTI) TMC125 is safe, well-tolerated and effective in HIV-positive patients with NNRTI and protease inhibitor resistance, according to data from two studies presented last week at the Tenth European AIDS Conference / European AIDS Clinical Society in Dublin. This indicates that TMC125 could be the first NNRTI that can be used after the development of resistance to other members of this drug class.

The currently available NNRTIs efavirenz (Sustiva) and nevirapine (Viramune) are potent anti-HIV drugs that can reduce viral loads and increase CD4 cell counts when used in combination with other antiretroviral agents. However, a disadvantage of these drugs is that only one mutation is required for HIV to become resistant to them, and that resistance to one drug leads to resistance to both drugs, preventing either from being used in the future.

TMC125 or etravirine is under development by the Belgian pharmaceutical company Tibotec and was designed to be active against HIV with pre-existing resistance to other NNRTIs. Previous studies have shown that TMC125 taken alone can reduce viral loads in patients with NNRTI resistance mutations.

For the studies presented in Dublin, investigators from Tibotec wished to assess the safety and efficacy of TMC125 in combination with other antiretroviral drugs in patients with substantial HIV treatment experience.

Safety and tolerability

In TMC125-C203, the first of two studies presented, the researchers randomised 240 patients to receive TMC125 at a dose of 400, 800 or 1200mg twice daily, or to receive placebo. TMC125 or the dummy pills were taken alongside an optimised background regimen consisting of at least two active antiretroviral drugs, which were chosen for each patient individually.

All of the patients had taken at least one drug from the three major classes of anti-HIV drugs for three months or more and were failing their current treatment regimen with viral loads above 1000 copies/ml.

The study was double blind, meaning that neither the patients nor the investigators knew which dose of TMC125 each patient was taking.

Overall, the patients taking TMC125 had comparable rates of side-effects to those taking placebo (92 vs. 91%). The commonest side-effects were diarrhoea (25 vs. 38%), headache (19 vs. 17%), rash (17 vs. 11%) and nausea (17 vs. 23%). None of these differences were statistically significant (p > 0.05).

The investigators found no significant differences in the rates of severe (grade 3 or 4) side-effects or laboratory abnormalities between the TMC125 and placebo groups, although the investigators were unable to conclude from the data available whether pancreatitis was associated with TMC125 or not due to the low number of cases they saw.

There were also no observable differences in the rate of side-effects between the three doses of TMC125 tested. However, the design of the study led to the patients receiving the highest dose of 1200mg twice a day being followed up for a median of 24 weeks, in contrast to 47 weeks for the 400mg group, 32 weeks for the 800mg group and 40 weeks for the placebo group. The shorter follow-up in the group receiving the highest dose may have led to an underestimation of the drug’s adverse effects at this dose.

The researchers wished to examine the incidence of rash and of nervous and psychiatric disorders in more detail, as these are major side-effects of the other available NNRTIs, nevirapine and efavirenz, respectively.

In contrast to nevirapine, TMC125 was not associated with an increased risk of rash across the three doses and in comparison to placebo, and the rate of rash was not different in men and women or in patients with different CD4 cell counts at the start of the study. The investigators concluded that only 8% of the patients had rash that was possibly related to TMC125, and these were generally mild or moderate in nature.

Similarly, the incidence of psychiatric disorders was similar in TMC125 and placebo groups (13 vs. 11%), as were the rates of nervous disorders such as headache, dizziness and insomnia.

“TMC125 was generally safe and well tolerated at doses up to 1200mg twice a day,” the researchers concluded. “No significant patterns of [liver toxicity] or neuropsychiatric disorders were detected.”

Efficacy and tolerability

The second study, TMC125-C223, set out to compare the antiviral efficacy of the 400 and 800mg twice-daily doses of TMC125 in patients with NNRTI resistance and three or more protease inhibitor resistance mutations.

The investigators randomised 199 patients to receive one of these doses in combination with a background regimen, or ‘active control’: the best available regimen from licensed antiretroviral agents. As in the first study, all of the patients were failing their current antiretroviral drug regimen, with a median viral load of 50,100 copies/ml and CD4 cell count of 99 cells/mm3.

After 24 weeks, the median reduction in viral load was 1.04 log10 for the 400mg group and 1.18 log10 for the 800mg group, under the assumption that the patients who did not complete the study experienced failure of the treatment regimen. In contrast, the patients taking the active control regimen had viral loads a median of 0.19 log10 below baseline. This was significantly less than in both TMC125 groups (p < 0.05).

These changes in viral load were mirrored by increases in CD4 cell count. While patients taking the active control regimens had a median increase of 10 cells/mm3, the patients taking TMC125-based regimens had increases of 47 and 48 cells/mm3.

“TMC125 is the first NNRTI to show significant activity in patients with prior NNRTI failure,” the investigators concluded. “TMC125 has the potential to be the first NNRTI to enable sequencable use of this drug class.”

The investigators also analysed the incidence of side-effects in this study. They repeated the findings of the earlier safety and tolerability study, finding no significant differences between TMC125 doses.

Comparisons between patients taking TMC125 and the active control could not be made due to many of the patients in the active control group stopping their assigned treatment early. After 24 weeks, 95% of the active control group had left the study, compared to 25% of those taking TMC125, with most of these being due to virological failure (75 vs. 6%).

Patients in the active control group who discontinued their assigned treatment went on to be offered TMC125 as part of a roll-over study.

Future directions

Based on the findings of these two studies, Tibotec selected the 800mg twice a day dose for future work. However, Julio Montaner and Jeffrey Nadler, presenting, revealed that the company has developed a new 200mg twice-daily formulation of TMC125. This tablet produces similar drug levels to the 800mg formulation used in these studies.

The new formulation is currently being studied in phase III trials of TMC125. Phase III trials are large, multicentre studies comparing a drug to a placebo or to the current standard of care. These trials usually form the final stage necessary before the drug’s developers can apply for its approval. Once the phase III trials of TMC125 are complete, they will indicate whether the drug will live up to its expectations by providing a new treatment option for patients who have experienced failure of NNRTI-based regimens.


Montaner J et al. Safety and tolerability of TMC125 in 3-class-experienced HIV-infected patients: 24-week primary analysis of trial TMC125-C203. Tenth European AIDS Conference / European AIDS Clinical Society, Dublin, abstract LBPS3/7B, 2005.

Nadler JP et al. Efficacy and tolerability of TMC125 in HIV patients with NNRTI and PI resistance at 24 weeks: TMC125-C223. Tenth European AIDS Conference / European AIDS Clinical Society, Dublin, abstract LBPS3/7A, 2005.


TMC126 PI Potent
NNRTI Potency similar to efavirenz
TMC278 NNRTI TMC278, an investigational nonnucleoside reverse transcriptase inhibitor (NNRTI) reputed to have a high barrier to resistance, passed a crucial step in clinical development—a 7-day monotherapy test in treatment-naive patients.[1] The median viral load drop measured 1.2 log10 copies/mL (more than 10-fold), reported Frank Goebel, MD, from Munich's Ludwig Maximilians University, at the 12th Conference on Retroviruses and Opportunistic Infections held in Boston, Massachusetts.  With activity against some NNRTI-resistant virus,[2] TMC278 is the second of 2 NNRTIs under development at Tibotec in Mechelen, Belgium. The drug's lengthy 38-hour half-life could make once-daily dosing possible.  Dr. Goebel and colleagues[1] in Russia and Britain randomized 47 treatment-naive individuals to placebo or 25 mg, 50 mg, 100 mg, or 150 mg TMC278 given once daily for 7 days as an oral solution. Study participants began treatment with a median viral load of 4.5 log10 copies/mL (range 3.5-5.9 log10 copies/mL) and a median CD4+ cell count of 292 cells/mm3 (range, 29-590 cells/ mm3).  After 7 days, the median HIV-1 load dropped 1.29 logs with TMC278 25 mg, 1.23 logs with 50 mg, 1.07 logs with 100 mg, and 1.17 logs with 150 mg , there was no change with placebo (P value vs placebo < .01 for all treatment groups). The apparent virologic equivalence between arms prompted speculation at the conference that an even lower dose may be possible. However, Dr. Goebel noted that longer treatment may distinguish between the doses.  No one stopped treatment because of toxicity in this brief study, and no serious side effects were reported. The median CD4+ cell count climbed 55 cells/mm3 in 7 days.  A multinational phase 2b dose-finding study begins in March 2005.
[CROI 2005:]
T-1249 Fusion
Not cross-resistant with enfuvirtide; possible once-a-day subcutaneous dosing; injection site reactions possibly less prominent (40%); rash and leukopenia are possible
Development stopped January 2004
SCH6 HCV PI May have significant activity against HCV
GW640385 PI Probably will be boosted with ritonavir; active against PI-resistant HIV?
RO033-4649 PI  
TMC-1142 PI Likely will be boosted with ritonavir.  May be active against many PI-resistant virus (1-3 primary PI mutations and resistance to up to 7 current PIs.) GI side effects. 


CCR5 antagonist Orally bioavailable; no activity against CXCR4+ HIV; expected launch 2008
BMS-378806 gp120
Produces a structural change in gp120; potentially active against CCR5 and CXCR4-binding viruses as well as subtype B HIV; orally bioavailable
BMS-4880431,2 Attachment inhibitor Oral compound with BID dosing which prevents the binding of the viral envelope protein gp120 to cellular CD4+ receptors.  In a small study up to 1 log decrease in viral load was noted; however, the rate of viral decay was widely variable among the subjects.
CCR5 antagonist Orally bioavailable.  No serious adverse effects noted.  Administration with food increased levels.  Expected launch 2008?

Following 10 days of twice daily monotherapy, the largest viral load reduction was seen in the 600 mg twice-daily group (mean decrease -1.6 log10 copies/mL). Reductions of -1.03, -1.23, -046 and -0.12 log10 copies/mL were seen in the 400 mg once-daily, 200 mg twice-daily, 200 mg once-daily, and placebo groups, respectively.3

This compound was removed from study in October 2005 due to excess hepatotoxicity.

Human monoclonal antibody to CCR5
GW8248 NNRTI Active against HIV with NNRTI-resistance mutations?
SPD-7542 NRTI Cytidine analog.  Enantiomer of previously studied DOTC. May be active against NRTI-resistant strains of HIV.  1200 and 1600 mg/day dosing produced >1.5log reduction in viral load.  No emergence of resistance mutations seen in one study.  Lamivudine markedly reduces the intracellular phosphorylation of this compound.
SM-309515  PI JE-2147 class of transition-state mimetic dipeptide HIV PI molecules
PRO 5421 Attachment
Expected launch 2008
CCR5 antagonist Oral CCR5 receptor antagonist.  Produces a 1-1.5 log viral load reductions at various dosages in a small trial.  One patient observed to have emergence of CXCR4 virus during trial.  Potential for drug interactions with other antiretrovirals.

This compound was removed from study in treatment naive patients in October 2005 due to lack of efficacy as compared to a standard regimen.

TNX 3551,2 Anti-CD4
A humanized anti-CD4 antibody, engineered by grafting murine proteins onto a human IgG4 antibody construct and then mutating amino acids in the framework to produce a structure that is 95% human.  Various dosages produced about a 1 log decrease in viral load, but by week 9, viral load had returned to baseline and resistance to TNX 355 had developed.  This may be the basis for designing similar therapies.
Under development for 10 years; prevents the last step of integration (strand transfer)
Sister drug to 812 above.
In a trial, 30 HIV-positive patients were given placebo (6 patients) or 200 mg or 400 mg of L-870810 (7 and 17 patients, respectively). Fifteen of the 24 patients given the drug were antiretroviral (ARV)-experienced.  After 10 days of twice-daily doses, the mean viral load decrease in the 200-mg and 400-mg doses was 1.73 and 1.77 log10 copies/mL, respectively (the latter is a 60-fold reduction in viral load). There was a wide range of response, from 0.95 to 2.49 log10 copies/mL, but no nonresponders. Six out of 16 patients on the higher dose (37.5%) had a viral load below 400 copies/mL by Day 10. After dosing was stopped, viral load increased again and was back to baseline by Day 24 in most subjects.  This was the last study that will ever be performed on this specific compound. Research on L-870810 has now been stopped after unacceptable liver and kidney cell toxicity was found in dogs. One of the reasons for the slow progress on integrase inhibition is that many candidates have turned out to be toxic and to inhibit other vital cellular functions.  However Little said that there was no evidence of human toxicity in the current study and that studies in rats had shown none. There were 4 discontinuations in this study; none were related to drug toxicity, and 3 were solely due to the suspension of the study when the dog toxicity data were released. Research on a related drug candidate L-870812 [above] is proceeding.
[CROI 2005:]
Extensive protein binding may be a problem
Development stopped early 20041

Cytidine analog.  Half-life of 17 hours suggests once a day dosing possible. Q151, 69 insertion, and K65R produce resistance to this agent.  50 mg, 100 mg, and 200 mg/day each produced about 1.7log reduction in viral load.  No significant adverse effects reported.

Hepatitis B Therapy

NRTI Cross-resistant with lamivudine; HBV resistance mutations selected in 19% after 2 years of therapy
entecavir NRTI Potent: 0.5 and 1.0 mg doses produce 2.8 and 2.5 log decreases in HBV DNA at 24 weeks and 3.8 and 4.4 log decreases at 48 weeks; 26% achieve undetectable levels at 48 weeks at both doses; best results with elevated transaminases at baseline; no significant adverse effects; effective against 3TC-resistance and in persons previously treated with interferon-alfa
telbivudine NRTI Additive or synergistic with lamivudine
clevudine NRTI  
famciclovir anti-HSV Less potent than lamivudine
thymosin thymic-derived peptides  
inhibit HBV nucleocapsid  

As of mid 2005, there are at least 83 antiretroviral therapies for HIV under development.

If readers have information pertinent to any antiviral investigational agents, please email me via the email address on the homepage of this site.

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Quick Menu / Table of Contents
Introduction Principles Management NRTI Info NNRTI Info
PI Info Fusion Inhibitors Drug Summary Investigational Adherence
Lab Evaluation Resistance Tests PEP Antiretroviral Tables OI Prevention
Vaccinations TB Therapy Hepatitis Therapy OI Diagnosis OI Therapy
Bibliography Links Palliative Therapy

Last Updated 11.25.2005

1 Rob Camp, Seven (Minus 4, Plus 3) Agents to Fix Your Gaze On March 2004

David Wohl, New Antiretroviral Drugs in Development, 2004

3 Keith Alcorn /

4 Gewurz BE, Jacobs M, Proper JA, Dahl TA, Fujiwara T, Dezube BJ.
Capravirine, a nonnucleoside reverse-transcriptase inhibitor in patients infected with HIV-1: a phase 1 study
J Infect Dis. 2004 Dec 1;190(11):1957-61. Epub 2004 Oct 27.