AIDS TREATMENT NEWS Issue #389, March 14, 2003
phone 800-TREAT-1-2, or 215-546-3776

CONTENTS

** Retroviruses Conference Clinical News: Interview with Cal
Cohen, M.D.
We asked a leading AIDS physician to summarize some of the
important treatment messages for physicians and patients, from
the 10th Conference on Retroviruses and Opportunistic
Infections, a major scientific meeting. Part 1 of the 2-part
interview looks at starting antiretroviral therapy (including
tenofovir vs. d4T, and efavirenz vs. nevirapine), new protease-
inhibitor information, and antiretroviral drug toxicity.

** First AIDS Vaccine Tested Did Not Protect, But Gives
Scientific Leads
AIDSVAX, the first HIV preventive vaccine to finish a human
efficacy trial, did not protect against infection, but is likely
to provide much information on designing better vaccines

** T-20: Most Expensive AIDS Drug Ever at $25,000 Per Year?
A new kind of HIV treatment will probably cost several times as
much as other AIDS drugs and be unavailable to many who need it.

** Clinton Team Lowers Drug Price 7-Fold in Caribbean
At the recent Retroviruses conference, President Clinton told
how his organization lowered the price the government of the
Bahamas paid for HIV treatment, from $3600 to $500 per year.

** Help Wanted: Treatment Information and Advocacy at Project
Inform, Spanish Bilingual Preferred
Resume requested by March 21, 2003.

** Warning, Counterfeit Procrit(R) (Epoetin Alfa)
The FDA and Ortho Biotech have warned health professionals and
patients to check for counterfeit Procrit, which may contain
dangerous bacteria and have no active ingredient.


***** Retroviruses Conference Clinical News: Interview with Cal
Cohen, M.D.

by John S. James

Cal Cohen, M.D., has been an AIDS physician since the mid 1980s.
Currently he is research director of the Community Research
Initiative of New England, and teaches at Harvard Medical School
in Boston, Massachusetts. He has a clinical practice in Boston
at Harvard Vanguard Associates.

We asked Dr. Cohen to discuss some of the most important
information from the 10th Conference on Retroviruses and
Opportunistic Infections, February 10-14 in Boston -- focusing
mostly on the news that physicians and patients can use now.

This is part 1 of the 2-part interview.

***

Dr. Cohen: Some of the clinical highlights of this conference
were:

* More proven options for beginning antiretroviral therapy;

* More information on switching antiretrovirals if necessary --
including possible options on delaying the switch until a better
new regimen is available, and also information on structured
treatment interruption;

* Reports on lipodystrophy, heart-disease risk, and other side
effects of some antiretrovirals;

* Viral resistance to drugs, and ways to minimize it; and

* New drugs in the pipeline -- a "bumper crop," as one prominent
researcher said.

Starting Antiretroviral Therapy

Dr. Cohen: At this meeting we saw more data about the
differences in the second year of taking d4T (Zerit(R)) vs.
tenofovir (Viread(R)).(1) About 600 volunteers were randomly
assigned to take one or the other of these drugs; in either case
they also took 3TC (Epivir(R)) and efavirenz (Sustiva(R)). The
trade-off presented was good news for tenofovir on safety; only
1% of the patients had lipodystrophy (as defined by the
researchers) vs. 12% for d4T. Tenofovir patients had less
neuropathy as well (not a surprise) -- and also a better lipid
profile. The safety certainly favors tenofovir. Yet many
patients can tolerate d4T; in this trial more than 80% of those
on d4T did not have visually apparent lipodystrophy even after
two years.

Is there some way to predict who is most vulnerable to
lipodystrophy? Researchers are working on that. And if
lipodystrophy does develop, how reversible is it? We have
learned at this and other meetings that it can be reversible,
especially if we catch it early enough.

The tradeoff on tenofovir plus 3TC (vs. d4T with 3TC) is what
may happen with resistance. If someone does develop virologic
escape from this tenofovir starting regimen, about 25% of the
time they will have the K65R mutation (but that was only about
1% of the patients in this trial -- see below). This mutation,
along with the 3TC resistance mutation M184V, can create
resistance to many of the other nucleosides, and leave only AZT
and d4T predicted to be active nucleoside drugs for people with
these mutations.

But with d4T plus 3TC, if you get resistance and viral rebound,
usually you only get resistance to the 3TC and less likely to
d4T, which has a different genetic barrier to viral resistance.
In the tenofovir vs. d4T trial above, of the 28 people who had
virologic escape, there were 2 cases of K65R on d4T and 7 with
tenofovir. So the difference is all of 5 people, in a study of
600 -- a difference of about 1% so far, having the additional
risk of getting the more serious viral resistance with the
tenofovir. Still this is the trade-off people need to consider -
- increased risk of lipodystrophy, vs. the extra 1% risk of
worse cross-resistance to nucleoside analogs.

One possible way to minimize both lipodystrophy and cross
resistance is for somebody to start on d4T for perhaps six
months, then switch over to tenofovir once their viral load is
clearly less than 50 copies, for example. Most important with
either regimen, however, is to make sure that the treatment is
working and suppressing the virus.

James: Even though d4T may work well for some patients, is it
still agreed that nobody should use d4T plus ddI, because of the
toxicity of the combination?

Dr. Cohen: Yes. While both drugs have uses separately in some
patients, they should not be used in combination.

Efavirenz vs. Nevirapine in Starting Regimens

Dr. Cohen: The so-called 2NN study (for 2 non-nucleosides) had
four arms. It compared efavirenz (Sustiva(R) in the U.S., also
known as Stocrin(R) in some countries), vs. nevirapine
(Viramune(R)) once a day, vs. nevirapine twice a day, vs. the
combination of efavirenz and nevirapine. All volunteers also
received d4T plus 3TC. This study enrolled over 1200 volunteers
in 17 countries in Europe, North and South American, Australia,
and South Africa.(2,3)

The first, easy conclusion is that there is no good reason to
combine nevirapine and efavirenz; that arm did not do better in
any important way, so we can forget that combination. In
comparing nevirapine once vs. twice a day, there was a
demonstration of more liver toxicity in the once a day arm vs.
twice a day. So it may be safer to consider nevirapine a twice a
day drug, even though in overall success they seemed about
equal.

What about comparing efavirenz vs. nevirapine, one main purpose
of this study? They were more similar than different but
technically not equivalent. Some prior studies have not done
well for nevirapine. This one, the first head-to-head comparison
with efavirenz, increased the data supporting nevirapine as a
decent drug.

The problem is the toxicity profile of nevirapine, including a
higher percent of liver toxicity with either once or twice a day
nevirapine than with efavirenz. Two deaths among the 800 or so
volunteers taking nevirapine in this study were attributed to
nevirapine [one from liver failure, the other from an
antibiotic-resistant staph infection acquired in a hospital
while recovering from Stevens-Johnson syndrome]. We have known
from other studies that there is a rare but potentially fatal
liver complication that occurs in the first weeks or months of
use of nevirapine. This was reported for example in the study of
FTC vs. 3TC done a few years ago in South Africa -- where
reports of very rare but fatal liver toxicity were noted. This
is another factor to consider as we construct the first regimen
for a patient.

James: Do we know from that study if the person who died of
liver failure was monitored correctly for liver toxicity?

Dr. Cohen: We do not know yet from the report at this
conference, and it would be helpful to learn from the company if
this occurred despite monitoring, or if this volunteer was not
monitored according to the protocol. It is important to know if
the recommended blood tests could usually find this liver
problem in time.

So on nevirapine this trial provides more data to inform the
choice. It does not tell us which drug is better.

It is still fair to say that Sustiva (efavirenz) is at least as
good as Viramune (nevirapine), and may be better in some ways.
There was nothing presented that made nevirapine a better choice
-- except for those who cannot tolerate the well-known efavirenz side
effects of vivid dreams and mood changes. Overall,
nevirapine is probably just as good or slightly worse on
average. The statistics for this trial allow us to state with
confidence that nevirapine is similar and no more than 12% less
successful than efavirenz.

Protease Inhibitor Information

Dr. Cohen: Within the protease inhibitors, we saw new data from
the drug 908, which is the reformulation of amprenavir. It did
much better than nelfinavir, and impressively it did well even
at much higher viral loads. It may be the best data we have seen
in an un-boosted protease inhibitor doing well at high viral
loads.(4,5,6)

It is not clear if clinicians will choose to use 908 earlier in
treatment (when this drug is approved), because there are some
lipid disturbances. But 908 certainly is interesting in the same
way that Kaletra is interesting, because not only is it very
potent, but also if you do get viral escape and rebound, boosted
protease inhibitors including 908 plus low-dose ritonavir did
help protect from resistance not only to the protease
inhibitors, but also to the other drugs in the regimen.

[Note: a "boosted" protease inhibitor means that the drug is
used in combination with another protease inhibitor -- often but
not necessarily a small dose of ritonavir, which slows the
body's metabolism of many drugs, thereby keeping the blood level
of the other protease inhibitor high. Kaletra (lopinavir plus
ritonavir) is automatically boosted, because it includes a small
ritonavir dose in the pill.]

One of the most attractive things about a boosted protease
inhibitor as a starting regimen is not only its potency, which
is clear and established, but also this high genetic barrier to
resistance. For some patients -- particularly those whose
adherence may be spotty or erratic -- the danger of using a non-
nuke (efavirenz or nevirapine) is that the patient might lose it
early in their treatment to viral resistance, due to poor
adherence. If someone might not be ready to start antiretroviral
therapy but wants to give it a try, there is something to be
said for the boosted protease inhibitor and taking advantage of
that high genetic barrier to resistance. (Of course, if someone
has side effects from ritonavir, for example gastrointestinal
upset, then the regimen becomes less desirable as a way to find
out if one wants to be on treatment. Therefore many physicians
prefer to start with two nucleoside analogs and a non-nuke for
beginning treatment -- another tradeoff to consider.)

Data on 908 had been presented earlier at the Glasgow meeting.
At the Retroviruses meeting, a poster provided data about the
lack of viral resistance on boosted 908.(6) The researchers did
not find protease inhibitor resistance in that arm -- and
indeed, found less resistance to the nucleosides as well. It
probably takes more non-adherence to get viral rebound on a
boosted protease inhibitor than on the other available
antiretroviral regimens. If you do rebound it is probably
because you stopped the drugs, not because you missed a few
doses.

A new experimental protease inhibitor -- atazanavir -- looks
attractive because of its lack of lipid disturbances. This drug
does not have a lot of the toxicities including insulin
resistance that have tainted protease inhibitors so far.(7)

The other piece of the puzzle on atazanavir can be seen as an
evolution of three stages of controversy around resistance and
cross-resistance.

The first-generation discussion was the nelfinavir vs. indinavir
battle, in which nelfinavir had a more salvageable pathway
(meaning better treatment options if resistance does develop to
the drug).

The second battle was the boosted PI, where no resistance
developed when those drugs were used.

And now we have a third version of the story, which is if you
use atazanavir first and get rebound, you actually get
hypersusceptibility of the virus to other protease inhibitors --
meaning that the virus is more susceptible to the drugs (at
least predicted, based on the mutations seen). The clinical
meaning of that is not yet known. But we do have information
about hypersusceptibility with other drugs, suggesting that it
does seem sometimes to make a difference. So it may or may not
sway clinicians to want to use it for that reason. And there are
controversies around whether atazanavir is as potent a drug as
we might need for some patients. There may be some patients with
a high viral load and low CD4 where you may not want to trust
atazanavir, at least with two nukes. It does add another layer
of controversy or complexity in what makes these regimens
attractive.

Overall, it was a very good meeting in making us feel that we
have more options than before, more attractive options, and
different ways to balance the tradeoffs. So we feel less stuck,
with more flexibility.

Antiviral Drug Toxicity

Dr. Cohen: This meeting also focused on blood cholesterol and
lipids, with analysis of data from a very large cohort of study
volunteers in Western Europe and the U.S., to see if there is
any evidence of increased risk of heart disease in those on
treatment. As you know, this analysis, called the D.A.D. study,
did find an increase of about 25% in the rate of heart attacks
[per year of exposure] in people on any antiretroviral
treatment.(8)

The limitation of this study, or at least the analysis done so
far, is that it did not sort out which drugs may be more likely
or less likely to cause heart disease. Given that HIV treatment
is needed, this study said there is a risk but did not say what
to do about it. It did not entirely answer whether the lipid
effect of treatment completely explains the problems -- meaning
that if you avoid the lipid problem then can you avoid the risk
(the alternative is that there is some other mechanism at work).
One of the surprising and confusing points of the analysis
presented is that they found that those who had lipodystrophy
had a *lower* risk of heart attacks. In general, drugs that
cause lipodystrophy tend to have more blood cholesterol and
triglyceride problems. So you have the paradox, in that one
effect of these drugs is to increase lipids, and the other
effect is to increase lipodystrophy, but these seem to go in
opposite directions on heart risk. So while there is cause for
concern, this trial does not yet tell us what to do -- other
than avoid smoking, since nothing has changed about that.

Choosing different drugs is still a question of trade-offs;
there is still no perfect regimen, although we get closer. At
this meeting, the news on the nucleosides was the differences
between them -- and particularly, since almost everybody
continues to agree that 3TC is such a good drug that it deserves
to be used up front, the question of which nucleoside you pair
with it.

Note: Part 2 of this 2-part interview will include treatment
interruption, "deep salvage" in very treatment-experienced
patients, an experimental human monoclonal antibody, and a brief
summary of some of the major take-home messages for doctors and
patients.

References

Unless otherwise stated the references are to the 10th
Conference on Retroviruses and Opportunistic Infections, Boston
February 10-14, 2003.

Note: You can find all of the following abstracts at the
official conference site, http://www.retroconference.org; they
will remain there for about a year. To find a particular
abstract, you can either search for the poster number, for an
author, or for a word in the title. You can also search by
subject -- by looking for all abstracts that contain a
particular key word, such as the generic name of a drug. In the
listing below we indicated if a poster is also available online
with the abstract (as of March 1, 2003, when we checked -- other
posters may be added later). Researchers were encouraged but not
required to submit online posters (for oral as well as poster
presentations), which have more information than the abstracts.
Usually these posters were submitted digitally, not as
photographs, so they can be seen and read clearly online.

The abstracts and posters should be readable on all computers,
but you need (1) to have the free Acrobat reader for the posters
(if you do not already have it, you can download it from
http://www.adobe.com/products/acrobat/readstep2.html), and (2)
to *not* have your browser's Internet security setting too high,
or the software to search the abstracts may not work.
(Unfortunately the Webcast sessions, also on the official site,
use a Microsoft format and can only be heard on Windows.)

1. S Staszewski, JE Gallant, AL Pozniak, and others. Efficacy
and safety of tenofovir DF (TDF) versus stavudine (d4T) when
used in combination with lamivudine and efavirenz in
antiretroviral naïve patients: 96-week preliminary interim
results. [Abstract #564b]

2. F van Leth, E Hassink, P Phanuphak, and others. Results of
the 2NN study: a randomized comparative trial of first-line
antiretroviral therapy with regimens containing either
nevirapine alone, efavirenz alone or both drugs combined,
together with stavudine and lamivudine. [Abstract #176]

3. F van Leth, P Phanuphak, B Gazzard, and others. Lipid changes
in a randomized comparative trial of first-line antiretroviral
therapy with regimens containing either nevirapine alone,
efavirenz alone or both drugs combined, together with stavudine
and lamivudine (2NN Study). [Abstract #752 - Poster available]

4. J Nadler, A Rodriguez-French, J Millard, and P Wannamaker.
The NEAT Study: GW433908 efficacy and safety in ART-naïve
subjects, final 48-week analysis. [Abstract #177]

5. E DeJesus, A LaMarca, M Sension, C Beltran, and P Yeni. The
Context study: efficacy and safety of GW433908/RTV in PI-
experienced subjects with virological failure (24 week results)
[Abstract #178]

6. S Macmanus, P Yates, S White, N Richards, and W Snowden.
GW433908 in ART-naive subjects: absence of resistance at 48
weeks with boosted regimen and APV-like resistance profile with
unboosted regimen. [Abstract #598 - Poster available]

7. R Murphy, V Pokrovsky, W Rozenbaum, and others. Long-term
efficacy and safety of atazanavir with stavudine and lamivudine
in patients previously treated with nelfinavir or ATV: 108-week
results of BMS study 008/044. [Abstract #555 - Poster available]

8. N Friis-Moler, R Weber, A D'Arminio Monforte and others.
Exposure to HAART is associated with an increased risk of
myocardial infarction: The D:A:D Study. [Abstract #130]


***** First AIDS Vaccine Tested Did Not Protect, But Gives
Scientific Leads

by John S. James

The first "phase III" trial -- one large enough to determine
whether a treatment works -- of an AIDS vaccine in humans found
that the vaccine (called AIDSVAX, produced by VaxGen in
Brisbane, California) failed to protect people from HIV
infection. But thousands of blood tests now being analyzed will
likely provide important information for making better vaccines.
Some of this work will be reported at the "HIV Vaccine
Development: Immunological and Biological Challenges" meeting
beginning March 29 in Banff, Canada.

Many scientists did not expect AIDSVAX to work, because this
vaccine only produces antibodies against HIV and does not
stimulate another branch of the immune system called cellular
immunity. Recently, however, there has been renewed interest in
antibodies -- partly because of growing knowledge about how to
select the right antibodies, and also because cellular immunity
alone may not prevent infection but only slow disease
development. HIV vaccines might need to use both.

The VaxGen report led to controversy because of suggestions that
AIDSVAX might work partially in Blacks, or Asians. In Black
volunteers, only 4 of 203 who received the vaccine later became
infected with HIV, compared to 9 of 111 who received the
placebo; in Asians the numbers were 2 of 20 vs. 2 of 53. There
is a widespread consensus that no conclusions about human
effectiveness can be drawn from such small numbers -- although
more research is needed to look for possible racial differences,
and this work has started. (This vaccine is not relevant to
Africa because it was made specifically for the clade B virus,
which causes the AIDS epidemic in the U.S., Europe, and some
other areas, but is not common in Africa, where AIDS is caused
by clade C and other clades of HIV.)

For more information on the science and controversy around the
February 24 VaxGen report, see:

* "Understanding the Results of the AIDSVAX Trial, by AVAC, the
AIDS Vaccine Advocacy Coalition, http://www.avac.org/, or
directly at:
http://www.avac.org/pdf/UnderstandingAIDSVAX.pdf (capitalization
*does* matter).

* Articles by Jon Cohen in SCIENCE magazine, February 28, 2003
and March 7, 2003 (and any following issues).


***** T-20: Most Expensive AIDS Drug Ever at $25,000 Per Year?

by John S. James

On February 24 Hoffmann-La Roche Ltd. announced a European price
for T-20, an experimental drug expected to be approved soon by
the U.S. FDA, probably in March 2003 [it was approved March 13].
The price, 52 Euros per day or almost $21,000 per year, is
expected to be close to the U.S. price, which will not be
announced until the drug is approved. If so, U.S. retail prices
are likely to be around $25,000 per year, several times the cost
of other AIDS drugs.

Roche said that the price "reflects the structural complexity of
Fuzeon and its highly sophisticated manufacturing process"
requiring more than 100 production steps. Trimeris, Inc. and
Hoffmann-La Roche Inc. (the U.S. branch of the Swiss company)
said that "U.S. patients currently enrolled in the FUZEON Early
Access Program will continue receiving FUZEON for free until it
is commercially available and participants' reimbursement can be
achieved." (Trimeris, Inc. is the small company that initially
developed T-20. It was then was acquired by Roche, which
financed the improved manufacturing, large clinical trials, and
other work needed for commercialization.)

The AIDS Treatment Activist Coalition (http://www.atac-usa.org)
said, "It is a tragic state of affairs in drug development when
an encouraging breakthrough drug cannot be accessed by the
people who need it most."

Comment

T-20 (also called FUZEON(TM), or enfuvirtide) is not a miracle
drug. It is about equally effective as other AIDS drugs, and
considerably more difficult to use, because it must be carefully
mixed by the patient, and injected twice per day. The advantage
is that T-20 is in a different class of drugs and works entirely
differently than other approved HIV treatments, so virus that
has become resistant to the other drugs is still susceptible to
T-20. Patients whose virus has become resistant need two or more
highly active antiretrovirals as a basis for a combination that
may get the virus under control again, and T-20 could be one of
those. But only a minority of patients would use T-20 even if
price were not an issue.

It is true that T-20 is difficult to manufacture and has been
expensive to develop. But how can the company get its investment
back if the price is so high that few of those who need the drug
(already a small market) can obtain it? Private insurance has
years of experience in getting rid of persons with HIV and other
expensive patients, who then end up in public programs. These
programs, like Medicaid and ADAP, are facing unprecedented
financial pressures and already cutting back. When they must
choose between providing T-20 or providing antiretrovirals to
four or five other patients who need them just as much, they are
unlikely to pay for T-20.

Much of the research and development cost of T-20 is really the
expense of developing expertise in a new field of
pharmaceuticals that is likely to be important in many areas of
medicine, not just HIV. Roche should accept that it is not going
to make all the money back on this one drug at any price.

In the future T-20 will likely be replaced by one or more small-
molecule drugs (from Roche, Trimeris, or others) that do the
same job with much less difficulty and expense. T-20 itself has
already provided the proof of principle, by showing that
patients can benefit from its action. Activists may need to make
sure that patent technicalities do not impede the development of
these different drugs by any companies.

Meanwhile, we fear that the cost of T-20 will force an issue
people wanted to avoid -- class differences in medical care.
Will we be moving toward separate treatment guidelines for those
who can and cannot pay?


***** Clinton Team Lowers Drug Price 7-Fold in Caribbean

by John S. James

On February 10, 2003, President William Jefferson Clinton gave
the keynote speech at the 10th Conference on Retroviruses and
Opportunistic Infections in Boston. As an example of the lack of
systems in place dealing with AIDS, he noted that his team
working in the Caribbean had in one week drastically lowered the
price the Bahamas paid for drugs:

"The week after we started working in the Bahamas we found out
that the government was buying, not from a big drug company, but
from a generic source, but through an agent or two, AIDS drugs
at $3,600 a year. Generically produced AIDS drugs at $3,600 a
year. Our people on the ground there, said, "This is nuts." They
went back and cut the deal directly with the manufacturer, and
in one week they went from paying $3,600 a year to $500 a year
per person, which means they're now serving more than seven
times as many people for the same amount of money, and another
1,000 people will live because of it. That's the good news. It's
a nice story, isn't it?

"It's horrible! Why does somebody have to drop in from another
country to figure out how to save 1,000 lives with the money
you're already spending? Why isn't somebody worldwide in charge
of this? When the South African drug case was settled, it turned
out to be largely a bust, because no one was put in charge of
figuring out how many people needed the medicine in which
countries, how much they could get it for, how much could they
pay, and who would close the gap. There has never been a system
to drive this.... We know that, without systems, madness like
this will happen. And since there are lots of countries that
cannot afford the $3,600 a year, there are a lot of people that
don't have medicine they would otherwise have. Nobody is in
charge of this deal. No one is in charge.

"So we're going to do what we can to make sure, in the countries
we touch, we give them a maximum chance to save more lives more
quickly. I hope that we can make a difference. I believe we can
tone up these systems very quickly, and move quickly from
treating scores of people to treating thousands of people."

Comments

Other activists could not expect such quick results. Besides
being a former president, Clinton's team had been invited to
help with AIDS in the Caribbean, and had signed a memorandum of
understanding with 15 governments there.

Today many people in poor countries still must pay several times
as much for generic antiretrovirals on the private market as
what the manufacturer sells them for. There is no rational
economic reason for such a large price increase -- thousands of
dollars per person per year to distribute a product that costs
so little to transport and store. Clearly the problems differ in
various countries and regions. Activists must look for ways to
overcome particular barriers, while also working toward workable
worldwide systems for distributing live-saving medicine.

Note: The full text of President Clinton's speech is at:
http://www.clintonpresidentialcenter.com/retroviral_2003.html


***** Help Wanted: Treatment Information and Advocacy at Project
Inform, Spanish Bilingual Preferred

Project Inform in San Francisco is seeking an Information and
Advocacy Associate "to research and write treatment information
for Project Inform publications and educational materials on
anti-HIV treatments, HIV-associated complications, and related
issues," and to work with other staff "to develop overall
information and advocacy priorities for the organization and to
participate in treatment advocacy efforts." Ability to speak and
write in Spanish is strongly preferred. A resume is requested by
March 21, 2003, but the job will remain open until filled.

The full announcement is available at:
http://www.projectinform.org/org/Jobs/index.html


***** Warning, Counterfeit Procrit(R) (Epoetin Alfa)

On March 12 the U.S. FDA and Ortho Biotech warned of counterfeit
Procrit, which is dangerous because the batches found are not
sterile, and have no active ingredient. The lot numbers are:
P007645 - 40,000 units/mL, Expiration 10-2004
P004677 - 40,000 units/mL, Expiration 02-2004
P004839 - 40,000 units/mL, Expiration 02-2004

These lot numbers were also used on authentic Procrit. Sometimes
the packages can be distinguished with the help of photos on the
Ortho Biotech Web site:
http://www.procrit.com/counterfeit/letter.html

Anyone finding suspicious product should contact the FDA's
Center for Biologics Evaluation and Research, 1-800-835-4709,
prompt #1, then prompt #5. Also call Ortho Biotech at 1-800-325-
7504.


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ISSN # 1052-4207

Copyright 2003 by John S. James. Permission granted for
noncommercial reproduction, provided that our address and phone
number are included if more than short quotations are used.

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John S. James
AIDS Treatment News
www.aidsnews.org