An Eye opener for Trial drugs

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An Eye opener for Trial drugs

Postby Melody » Tue Mar 14, 2006 5:45 pm

Six men in intensive care after drug trial
Tue Mar 14, 2006 11:41 PM GMT
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By Peter Griffiths

LONDON (Reuters) - Six men were seriously ill in a London hospital on Tuesday after taking a new drug during a clinical trial, health officials said.

The volunteers fell ill after taking a drug being developed to treat chronic inflammatory conditions and leukaemia, a medicines watchdog said in a statement.

The Medicines and Healthcare products Regulatory Agency (MHRA) said eight men took part in the trial, two of whom were given a placebo. The six who took it became ill.

U.S. drug research company Parexel International Corp. said it had set up the trial for German pharmaceutical company TeGenero AG.

"It is assumed that the adverse affects were based on a drug reaction," Professor Herman Scholtz, head of Parexel International Clinical Pharmacology, said in a statement.

"Such an adverse drug reaction occurs extremely rarely and this is an unfortunate and unusual situation."

Parexel said those who fell ill were taking part in the first human tests of an experimental drug called TGN 1412. It is being developed by TeGenero to treat diseases such as cancer and rheumatoid arthritis.

All regulatory, clinical and medical guidelines had been followed during the trial, Parexel said.

The MHRA watchdog said it had suspended the trial and notified other European regulatory bodies about the incident.

"Our immediate priority has been to ensure that no further patients are harmed," Kent Woods, MHRA's chief executive officer, said in a statement.

"We will now undertake an exhaustive investigation to determine the cause and ensure all appropriate actions are taken," Woods said.

The unnamed patients were moved to a critical care unit at the Northwick Park Hospital in north London on Monday from a research centre on the same site.

"They are in a serious condition," said Ganesh Suntharalingam, the hospital's Clinical Director of Intensive Care. "Their families are very concerned, and we are keeping them closely informed about their relatives' progress."

(Additional reporting by Gideon Long in London)
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Re: An Eye opener for Trial drugs

Postby HarryZ » Tue Mar 14, 2006 6:46 pm


Sure sounds like somebody didn't do their homework on this drug before giving it to these patients!!

Not very often do you read about such horrible results for a trial drug. I hope all these patients recover.

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Postby SarahLonglands » Wed Mar 15, 2006 4:27 am

Ironically, they weren't even ill before thay started the trial, but were just paid to see how they responded to the drug.

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Postby bromley » Wed Mar 15, 2006 1:44 pm

The following article suggests that the drug was being considered for MS.

Fingers crossed for the six men.

Drug trial halted after six volunteers hospitalised 15 March 2006

LONDON A British drug test has been stopped after six volunteers were hospitalised with severe reactions.

Two of the men are in critical condition in a London hospital and four are in serious condition.

All of them had taken a new drug as part of a clinical trial, which has now been suspended. The two other men in the trial had been given placebos.

The drug was being tested for treatment of multiple sclerosis, rheumatoid arthritis and leukemia. The German company that developed it says the pre-clinical trials all indicated the drug was safe and the adverse reactions were completely unexpected.

British health officials are now investigating.

Copyright 2006 Associated Press. All rights reserved
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Postby Dunmann » Thu Mar 16, 2006 7:37 am

Another article about this.

Treatment works by producing antibodies
By Nic Fleming, Medical Correspondent
(Filed: 16/03/2006)

TGN1412 was developed as a treatment for immunological diseases such as multiple sclerosis, rheumatoid arthritis and certain cancers.

The drug provides the body with extra antibodies - substances produced by the immune system. These bind to malfunctioning immune system cells.

Researchers at TeGenero AG, the small German pharmaceutical company behind the drug, believe it has promise as a treatment for B-cell chronic lymphocytic leukaemia, a blood cell cancer.

Preclinical studies suggested the drug had potential to reduce infection and improve control of cancer by stimulating the activity of T-lymphocytes (T cells) - white blood cells.

It was also proposed that TGN1412 could be used to switch off T cells involved in auto-immune diseases such as rheumatoid arthritis.

Last March the European Medicines Agency awarded TGN1412 "orphan medical product" status - a designation for medicines that could potentially be used for rare, life-threatening diseases for which no sufficient effective treatment exists.

The designation, which does not allow a company to market a drug, provides benefits such as reduced fees and advice on the conduct of clinical trials.

TGN1412 is a "monoclonal" antibody therapy. It is mass-produced in a laboratory by fusing a type of bone marrow cancer cell called a myeloma from a mouse with a white blood cell called a B cell, also from a mouse.

This produces a cell called a hybridoma that perpetually produces antibodies. Because the antibodies are identical clones produced from a single mono hybridoma cell, they are called monoclonal antibodies.

Monoclonal antibodies that react with specific antigens on certain types of cancer cells can be produced.

In recent years researchers have identified a growing number of cancer-associated antigens and clinical trials for a number of monoclonal antibody therapies are in progress. Regulatory authorities have approved treatments of this kind, including Herceptin for breast cancer and Avastin for colo-rectal cancer.
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Postby dignan » Fri Mar 17, 2006 11:36 am

Another update from New Scientist...

Catastrophic immune response may have caused drug trial horror

17 March 2006 - news service - A catastrophic over-stimulation of the immune system may have caused the horrific reactions suffered by six men taking part in the first human clinical trial of an experimental drug.

An investigation by New Scientist suggests the drug may have caused a super-immune response – sending white blood cells called T cells rampaging through the body destroying its own tissues.

Several experts contacted by New Scientist agree this is the most likely explanation for the terrible incident which put all six men in hospital intensive care in London, UK, with two in a critical condition. The victims, who were healthy, paid volunteers, are said to have suffered multiple organ failure.

The drug, called TGN1412 and made by German pharmaceutical company TeGenero, works by stimulating T cells, which could help treat leukaemia and auto-immune diseases such as rheumatoid arthritis. But this super-stimulation may have backfired. Indeed, a scientific article, highlighted on TeGenero’s own website, may have presaged this.
"Indiscriminate attack"

TGN1412 is a monoclonal antibody but works slightly differently from other similar drugs. It is a “superagonist”, causing a far greater immune cell response. It also does not require a second, specific trigger to kick-start this response, as do other monoclonal antibodies affecting the same T cell receptor.

“Fortunately, this [super-stimulation] does not occur naturally, because T cells activated in this way would lack any antigenic specificity and could indiscriminately attack normal tissues,” wrote Peter Linsley, from Rosetta Inpharmatics in Seattle, US, in March 2005 in a commentary accompanying a paper in Nature Immunology, which involved TGN1412.

“One could certainly say that, based on what [TeGenero] has already said about TGN1412, the most plausible explanation would be the triggering of a non-specific activation of natural killer T cells leading to indiscriminate cell destruction," says Ken Campbell, clinical information officer at the Leukaemia Research Fund in London, UK. "This would be consistent with multiple organ failure.”

An immunologist contacted by New Scientist, but who asked not to be named, says: “You don’t need to be a rocket scientist to work out what will happen if you non-specifically activate every T cell in the body.”

Michael Ehrenstein, at University College London, UK, who works on regulatory T cells and rheumatoid arthritis, believes the drug was intended to activate regulatory T cells. This subgroup of T-cells actually suppresses the activation of the immune system and stops it from attacking a person’s own body. TeGenero states that this is the strategy they hoped would ease the symptoms of rheumatoid arthritis patients.

“It’s possible there was contamination” of the drugs the patients received, Ehrenstein notes, but he says it is just as possible that something unexpected happened. “Instead of damping down the immune system, it’s activated it more. That’s what it looks like to me,” he told New Scientist.

Multiple attempts to contact TeGenero by New Scientist were unsuccessful. Previous experiments on immuno-deficient rats by the company indicated that the effect of the drug on regulatory T cells was disproportionately greater than on other T cells, leading to a normally functioning immune system. But it is unknown whether TGN1412 had been made more specific to regulatory T cells before the human trials.

Reports from friends and relatives describe the nightmarish symptoms suffered by the men. One man’s head was said to have swollen massively and his limbs turned purple. Another was said to resemble the deformed “Elephant Man”.

TGN1412 was being tested as a treatment for a range of illnesses, including autoimmune diseases, but it had been awarded special status as a possible treatment for a type of leukaemia called B-cell chronic lymphocytic leukaemia (B-CLL).

The drug is a type of monoclonal antibody. Antibodies are produced by the immune system in response to a foreign invader like a bacterium. It recognises the particular invader, or antigen, and neutralises it as well as kick-starting a wider immune response. A monoclonal antibody is one manufactured to be specific for one antigen only. These have been used safely in treatments for a variety of diseases, including lymphoma, experts stress.

But TGN1412 differs from other monoclonal antibodies because it is a superagonist – massively enhancing the body’s immune response. It works by binding to a molecule, or receptor, on the surface of a T cell called CD28. Normally, binding to CD28 triggers the T cell response, but only when the T cell is also bound by another factor which is specific to the tissue designated for attack.

However, TGN1412 bypasses this so-called “co-stimulation”. It binds in a different place on the molecule to natural antibodies and directly causes CD28 to provoke a strong T cell response, without needing the other antigen-specific molecule to bind.

This is what was highlighted by Linsley in his article accompanying the Nature Immunology paper (vol 6, p 271). In that paper, scientists had for the first time managed to crystallise and examine the structure of CD28.

Whatever the cause of the terrible side-effects seen in the UK trial, it is unusual not to have seen anything similar in animal testing, says Campbell: “CD28 is widely conserved across species. It’s very, very strange if it does turn out to be some idiosyncratic case in humans,” he told New Scientist.

The company insists animal testing gave no hint of these side effects. “These events were completely unexpected and do not reflect the results we obtained from initial laboratory studies which enabled us to progress investigations into human volunteers”, said CEO Benedikte Hatz, in a statement.

The UK’s regulatory body, the Medicines and Healthcare products Regulatory Agency, which halted the trial, is currently conducting an investigation which could take weeks to reach a conclusion.

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Postby Melody » Fri Mar 17, 2006 3:18 pm

Survivor guilt for beating drug bullet
Jonathan Este, London
March 18, 2006
THEY dosed the men at two-minute intervals. But five minutes after the human guinea pigs had been given the TGN1412, the drug trial started to go dramatically wrong.

The man who had been injected first suddenly started to complain about being hot. He took off his shirt but then he started to shake violently.

Minutes later the third of the six men trialling the anti-inflammatory drug started to vomit. Shortly after that No4 said he could not control himself and needed the toilet. He collapsed before he could make it.

Within minutes, six of the eight men who were trialling the drug were showing dramatic and disastrous reactions, a situation that none of the doctors at the London clinic were prepared for.

Two days later, four of the men are reported to be "improving" while two others remain in a critical condition.

One of those two, Ryan Wilson, a 21-year-old apprentice plumber from north London, reportedly begged doctors to "put him to sleep" as the pain became too intense to bear. His relatives were already grieving last night after they were told he had suffered heart, lung and kidney failure.

"They say they cannot give us any hope," Mr Wilson's sister-in-law, Jo Brown, said. "They have no idea how to treat him because they know nothing about the drug he's been given. It doesn't look good."

Myfanwy Marshall, from Adelaide, whose 28-year-old boyfriend is also fighting for his life, said she barely recognised her partner who she described as looking like "the Elephant Man".

"He is largely lifeless," she told journalists. "I can't even get an eyelid movement or a squeeze from his hand. He is a shell of who he is. He is completely puffed up, his face, his body; he is like the Elephant Man.

"When I walked in there, I expected to see his small face and curly black hair but he looks like a monster. He has tubes up his nose, in his heart, liver, lungs, neck and hands. They told me he could be like this for six months to a year.

"They tried to pump the drug out of his system but all his internal organs are infected. They said he could die at any moment. He needs a miracle."

Ms Marshall has retained a lawyer who said the drug companies could be held responsible for the injuries suffered by the volunteers.

"It's commonplace for drug companies to pay people who are involved in clinical trials small amounts of money such as this," solicitor Anne Alexander said.

"The fact this has gone so disastrously wrong and will result in a very detailed investigation does not enable the drug companies to avoid any obligations they've got."

The eight men had been offered pound stg. 2000 ($5000) each to test TGN1412 - a drug designed to treat leukemia, rheumatism and multiple sclerosis - which is made by pharmaceutical company TeGenero AG, based in Wurzburg, Germany, and was being tested at the London clinic by US research firm Parexel.

Raste Khan, who was the second to be administered with a drug, which turned out to be a placebo, described the scenes in the clinic's ward as "a living hell" that became a "vomiting bath" as one by one the men who had been given the actual TGN1412 started to show violent side effects.

"People were fainting and coming back to consciousness. The gentleman on my left was screaming, saying his back was hurting. It was horrible. It was terrifying because I kept expecting it to happen to me at any moment. But I felt fine and didn't know why. An Asian guy next to me started screaming and his breathing went haywire as though he was having a terrible panic attack.

"They put an oxygen mask on him but he kept tearing it off, shouting 'Doctor, doctor, please help me!' He started convulsing, shouting that he was getting shooting pains in his back.

"I feel guilty that I had the placebo. It was like Russian roulette. I was doing it for the money.

"But pound stg. 2000 is not worth your life."

Ms Brown said she could not recognise her young brother-in-law, Mr Wilson. "His head had swollen to nearly three times its normal size," she said. "His neck was the same. It was wider than his head and his skin had turned a dark purple. At first none of us recognised him. He looked nothing like the Ryan we know and love. His nose was spread across his face like it had been squashed.

"Ryan had tubes in his nose and mouth and was hooked up to a machine helping him breathe and to a kidney dialysis machine. His eyes had been Sellotaped up and he had been sedated. The doctors told us Ryan begged them to put him to sleep because he was in so much pain. He was in agony. Our fear is that he may never wake up." An inquiry is under way on the manner in which the drug was administered and whether the trial should have gone ahead at all. TeGenero had reportedly never tested its products on humans before - and it emerged that the American testing company, Paraxel, had initially been refused permission to test the TGN1412 because of safety fears.

TeGenero's chief scientific officer, Thomas Hanke, who said the company was "devastated" by the tragedy, said the new drug had shown no side effects when tested on animals. However, lawyers acting for one of the victims at Northwick Park hospital, northwest London, raised doubts about the animal experiments that TeGenero claimed to have carried out.

The Sun reported that a dog had died after being administered with the drug, but neither the testing firm nor the drug's manufacturer confirmed this.

The clinic has called for help from international experts in immunology and toxicity in an attempt to understand the dramatic and life-threatening symptoms.

Ganesh Suntharalingam, the clinic's director of intensive care, said that some symptoms were recognisable, but the overall reaction was not.

It was too early to say whether the men would make a full recovery.

"There is an inflammatory process going on that seems to have been triggered by something - that process started to affect other parts of the body so we have two jobs to do," he said.

"One is to try to treat the inflammation and the other is to deal with the consequences of it."

The investigation will focus on the manner in which the drug was administered.

John Henry, a clinical toxicologist at St Mary's Hospital, London, told reporters: "The dose they were using is the whole key here. What was their target dose and what did they start with?

"They should have started with a minuscule dose and given it to the first two volunteers to see if there was any reaction. Then they should have moved on to the next two volunteers and multiplied the dose. You can't, in all conscience, give six people the same dose and hope they will all react perfectly.

"It is just common sense."

The head of a testing company, who asked not to be identified, said the drug-testing industry was "praying" that the incident had been the result of a human error.

"If it is not due to human error then it means that you can take a new molecule through discovery and laboratory testing, through all the animal studies and see nothing untoward until you take it into man at a minuscule dose and you see a catastrophic event.

"That would undermine the testing and development of all new medicines."

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Postby OddDuck » Sat Mar 18, 2006 7:37 am

This whole thing makes me ill (again). Here is why:

Simply put: As I have unpopularly opined in the past, messing with mab's is a scary proposition (at least to me, it is).

To quote from the article(s) below with regard to TGN1412:

..."There is an inflammatory process going on that seems to have been triggered by something - that process started to affect other parts of the body so we have two jobs to do," he said.

"One is to try to treat the inflammation and the other is to deal with the consequences of it."


"...An investigation by New Scientist suggests the drug may have caused a super-immune response – sending white blood cells called T cells rampaging through the body destroying its own tissues. ..."

No kidding!!

Anti-CD28 (downregulating and/or modifying) has direct effects on IL2, IL4 and IL10. From the additional research I've been doing, TGN1412 basically ends up blocking the activation of IL2, and drastically raises IL4 and IL10.

Now, here is the danger that I was afraid of and voiced (with regard to daclizumab, though, which is similar) regarding what might (or probably would) happen if you blocked the activation of IL2.

In our thread ... 25&start=0 , I explained my concerns with regard to inhibiting IL2, some of which were (you might be interested in going to that thread and reading more):

....The increase in "bacterial" infection. BAD news!! I researched further. The particular "bacterial" infections that are connected with inhibited IL-2 are from "superantigens". In other words, things like TB, borrelia, systemic infection, toxic shock, sepsis, things like that. MANY bacterial infections in the world, as you know, are already becoming resistent to antibiotics, and death often happens pretty quickly. And many of these everyday bacteria that we all are exposed to are held in check in everybody's body by our immune system. Bottom line, held in check by IL-2. And this concern doesn't even take into consideration what we already know is the risk that is being run, when being treated with immunosuppressants, from the possible increase or activation of viral infections. ...

...Messing with IL-2 can be nasty. Real nasty. Again, in organ rejection, it can be and is needed under very close monitoring (it is even suggested via hospitalization) and most often for short-term use. But in or for a basically non-fatal disease like MS? Pardon my scoff, but...........yeah, right!!! ...."

Now, on top of blocking IL2, TGN1412 also raises IL4 drastically. In another discussion with regard to IL4 (which I have always called a "double-edged sword") at ... hlight=il4 , we talked about (forget about desipramine for the moment and just focus on what I was talking about with regard to messing with IL4):

...Yea, usually IL-4 and IL-10 work in concert (at least that's what I found from my reading habits..... ), but they aren't dependent upon one another, which I believe is a good thing in MS for purposes of immune modulation.

The thing is, in MY opinion (and I ran across this while researching the drug desipramine and hence why I went off on sidelines regarding individual cytokines) that you want to raise levels of IL-10 (anti-inflammatory, and it helps to reverse the blood/brain barrier permeability); but lower levels of IL-4 for reasons of inhibiting CD4 attacks on myelin, and IL-4 enhances MHCII binding (APCs), so again, keeping IL-4 lower should (note I say "should", this again is totally unproven, and still controversial) also be adjunctive and beneficial because you definitely want to regulate MHCII. Higher levels of IL-4 correlates with lymphoma, also. Keeping IL-4 on the low end (or perhaps maintaining status quo levels of IL-4 in MS, once it is determined what the optimum levels of IL-4 should be in MS) helps to maintain or increase VIP. Without going into another long dissertation about VIP/PACAP, I'll quote from my original research: VIP/PACAP contributes to the initiation of TH2-type immunity, whereas in the presence of a full-blown, inflammatory reaction, VIP/PACAP act as anti-inflammatory agents.

Keeping the immune system predominantly on the TH2 side of the equation is desirable (from what I can find) in MS (whether that holds true in ALL patterns of MS, is yet to be determined).'s the odd part about IL-4. There ARE different suppositions about IL-4 in MS. Copaxone, for one, raises levels of IL-4 and IL-10. Interferon appears to maintain or decrease levels of IL-4. The problem with the interferons in my mind (which is another topic of discussion) is that it was found that over time IFN-beta 1b also increases some pro-inflammatory cytokines, IL-6 for one, which is part of the problem that contributes to the side-effects, and apparently could potentially counteract its beneficial immunomodulatory effects. Odd, huh?

I found that desipramine decreases (or maintains) IL-4 and increases IL-10. Both, in MY sole opinion, to be desirable for MS treatment (or therapy, if it can ever be ascertained via clinical trials on MS).

Plus, this is only pertaining to the immune side of the equation in MS (or some forms of MS). The genetic, environmental toxin, and pathogen sides, which are also pieces of this complex puzzle, aren't even factored in with this.

I still say to clinical researchers everywhere: Do an ELISPOT on each of your MS patients periodically, so we can correlate the findings and see what we come up with! That just MIGHT weed out a few, anyway, of the ongoing theories over cytokines and MS, correct?...

During different types of infection(s), etc., the body NEEDS some of the inflammatory cytokines in order to fight the infection off. Some of those viruses and/or bacteria are ones that our body already has inside us lying dormant due to the fact that our immune system is constantly regulating and keeping them in check. Now, if you raise IL4 TOO drastically, you basically are inhibiting the inflammatory cytokines to activate in order to fight infection(s). Some inflammatory cytokines you just plain do need now and again. And as we speculated above some time ago, IL4 is a double-edged sword, so basically "balance" of IL4 might be the key word there.

Now, put these two things together. If you drastically inhibit IL2, as we see above, you run the risk, almost immediately, of infections (virus and/or bacterial both) to run rampant. Then add raising IL4 at the same time?? So, now you not only have something like sepsis or a systemic (inflammatory) infection going nuts, and since you ALSO have IL4 stopping the immune system from activating any other "inflammatory" cytokines to help fight the infection, what will likely happen? The lack of IL2 has caused an extreme inflammatory reaction and having too much IL4 keeps your immune system from coming to the rescue. Double jeopardy. Common sense should dictate that everybody should have given concern to what I worried about above some time ago.

And what are they saying appears to have happened to those poor people who took TGN1412? Pretty much what I was concerned about and why I warned about it with regard to daclizumab. But, I have to say TGN1412, due to its "super" profile, turned out to be even more dangerous. But............if I could put two-and-two together as a simple equation, why didn't they??

Some speculations that I have read, but no proof yet, is that due to the multiple organ failure of the people who took TGN1412, it is appearing as if there was a sudden systemic infection (or sepsis). Just as I was afraid might happen if you block IL2 ALONE, nevertheless if you also raise IL4 too much at the same time! Especially in healthy volunteers????

This should give the researchers a red flag for the future while messing with mab's. First Tysabri, now TGN1412.

I'm not saying the mab's may not be helpful, they can be. But, why is it that someone as dumb as I am can see the probable handwriting on the wall just from my simple two plus two common sense equations, and the experts can't predict a thing? :evil:

I wish those poor people well.

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Re: An Eye opener for Trial drugs

Postby NHE » Sat Mar 18, 2006 8:10 pm

I watched some news coverage of this event last night. They interviewed a potential trial participant. This man stated that he felt he was being pressured to sign the release form without reading it. He stated that he was told "... if you just sign it then we can get on with the trial." He felt uneasy about being pressured into signing the release form without reading and understanding it so he declined to participate in the trial. My personal reflections are that it sounds like these researchers are better suited for selling used cars than conducting medical trials with human participants. The arrogance of the whole situation is also beyond comprehension. Evolution has perfected the immune system and the recognition of self vs. non-self and these people thought they could just bypass it and proverbially whack it with a big stick?

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Postby JFH » Mon Mar 20, 2006 1:23 pm

A strange report today. It seems that contrary to expectation the number of people volunteering for clinical trials has increased in the UK since this debacle. Because ... it wasnt generally known that you can get paid for taking part!
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