About ERIX
EiRx Therapeutics is a specialist provider of pre-clinical therapeutics to the pharmaceutical industry. Our unique scientific expertise and knowledge in the field of Apoptosis provide a sound base to discover and develop new medicines that will safely and selectively repair this natural process in disease. The potential benefits from these new medicines are enormous, since as many as 70% of all human disease have some defect in the control of Apoptosis.
Apoptosis - the biological process that determines whether cells in our bodies live or die...
http://www.eirx.com/index.html

Purchased some of these on the strength of the PROGRESS UPDATE looks promising.
http://moneyam.uk-wire.com/cgi-bin/articles/200603200701130254A.html

ERX interview with John Pool
http://www.wallstreetreporter.com/interview.php?id=18589&player=real
Latest News
CANCER COLLABORATION WITH BIOMERIEUX SA
http://moneyam.uk-wire.com/cgi-bin/articles/200607120700230534G.html
Biomerieux Web Site
http://www.biomerieux.com/servlet/srt/bio/portail/home
ABOUT ERX Focus Of The Month
http://www.billamag.net/focus-document-text.asp?FocusTextID=1
ERX pdf filehttp://www.eirx.com/eirx_heading_images/Yokohama2005.pdf
19/09/2006 A 50% reduction in breast tumour volume size seen with Eirx lead molecule in animal studies
http://moneyam.uk-wire.com/cgi-bin/articles/200609190700171175J.html

Past and present collaborative partners include:

* bioMieux SA
* Almac Diagnostics Ltd
* Merck & Co, Ltd
* Biofocus plc
* MGI Pharmaceuticals, Inc
* OSI Pharmaceuticals, Inc
* Sareum plc
* Regen Therapeutics plc
* SR Pharma plc

going to get more at .0017p I hope

PH

I GOT IN AT .24 and was just going to sit and wait as a long term hold,but might buy more if it drops, ??

I know I will, we already know news is around the corner.. its expected this month..

cheeky mm; knocked the price down, they then bought and then whacked the sp right up.. talk about a rip off merchants

Riskypete ... ERXBuy

That's no recommendation, he writes on a bb and uses the same texts as you.

sww

I tend to agree with your first post ! there is a lot of similar research going on .

I don't want to star a fight, but I feel ph is one and the same risky pete.

The bargepole is now in full use.

no.. I am not, I am cannon over at AD fvn .com

Gentium to Present Data Showing Defibrotide Modulates Immune Functions; Endothelial Cell Protection and Anti-angiogenic Activity Has Impact For Transplantation And Cancer Therapy


VILLA GUARDIA (COMO), Italy--(BUSINESS WIRE)--Sept. 5, 2006 - Gentium S.p.A. (NASDAQ:GENT) (the Company) today announced that Gunther Eissner, Ph.D., Department of Hematology, Regensburg University Medical Center, Regensburg, Germany, and Massimo Iacobelli, M.D., Senior Vice President, Scientific Director, Gentium, S.p.A., will make an oral presentation entitled, "Defibrotide Modulates Immune Functions Of Endothelial Cells - Impact For Transplantation And Cancer Therapy," at the 16th European Congress of Immunology. The Congress is being held from September 6-9, 2006 in Paris, France. The presentation will take place on Thursday afternoon, September 7, 2006 in the Immune Interventions Workshop--Immunohematology Track D section in Room 251 at 3:00 p.m. local time.

In their presentation, Drs. Eissner and Iacobelli will show evidence that Defibrotide can protect endothelial cells from conditioning-mediated apoptosis, which suggests that the drug may be used as a prophylactic in patients at risk for endothelial complications. The evidence demonstrates that Defibrotide has anti-inflammatory activity because it prevents transendothelial migration of immune effector cells, and it can reduce the chemotherapy-induced antigenicity of endothelial cells towards allogeneic cytotoxic T lymphocytes.



In addition to these endothelium stabilizing functions, recent pre-clinical evidence suggests that Defibrotide has anti-neoplastic properties, which may be due to its ability to prevent tumor angiogenesis. The anti-angiogenic potential of Defibrotide was tested in vitro using a novel angiogenesis kit (AngioKit(TM)) and in vivo using the dorsal skin fold chamber model in mice. The results demonstrated that Defibrotide at concentrations corresponding to pharmacologic Defibrotide blood levels (100 ug/mL) reduces blood vessel formation significantly (p=0.022), when administered on a daily basis. Furthermore, Defibrotide significantly reduced tumor angiogenesis in the murine dorsal skin fold chamber after inoculation of cells from the human gastric cancer TMK. Regarding the mechanism of action of Defibrotide, initial Western blotting results show that Defibrotide reduces phosphorylation-activation of p70S6 kinase, which is a key target in the PI3K/Akt/mTOR signaling pathway linked to angiogenesis. Additional in vitro data suggest that Defibrotide's action is independent of a blockade of vascular endothelial growth factor (VEGF).

Dr. Laura Ferro, Chairman and Chief Executive Officer of Gentium, commented on the presentation, "The pre-clinical data demonstrate Defibrotide's activity in multiple pathways. Taken together, the data suggest that while Defibrotide is known for its endothelium-protecting function, it also can inhibit blood vessel formation. These data support our clinical strategy to pursue further testing of Defibrotide as an anticancer agent, either as a monotherapy or in combination with other drugs, especially as it appears that it can work synergistically with other VEGF-dependent, anti-angiogenic substances."

About VOD

Veno-occlusive disease (VOD) is a potentially life-threatening condition. Certain high dose chemotherapy and radiation therapies and stem cell transplantation (SCT) can damage cells of the blood vessels and result in VOD, a blockage of the small veins of the liver that can lead to liver failure and the failure of other organs (Severe VOD). SCT is a frequently used treatment following high dose chemotherapy and radiation therapy. The International Bone Marrow Transplant Registry estimated that approximately 45,000 people received blood and bone marrow transplants, which are types of SCT, in 2002. Based on the Company's review of more than 200 published papers, it believes that approximately 20% of patients who undergo SCT develop VOD, approximately one-third of those who develop VOD progress to Severe VOD, and approximately 80% of Severe VOD patients die within 100 days of the SCT. The Company believes that there are no approved therapies to treat or prevent VOD in the U.S. or the EU.

About Gentium

Gentium S.p.A. is a biopharmaceutical company located in Villa Guardia (Como), Italy that is focused on the research, discovery and development of drugs derived from DNA extracted from natural sources, and drugs that are synthetic derivatives, to treat and prevent a variety of vascular diseases and conditions related to cancer and cancer treatments. Defibrotide, the Company's lead product candidate in the U.S., is an investigational drug that has been granted Orphan Drug status by the U.S. FDA to treat Severe VOD and Fast Track designation for the treatment of Severe VOD in recipients of stem cell transplants.

Cautionary Note Regarding Forward-Looking Statements

This press release contains "forward-looking statements." In some cases, you can identify these statements by forward-looking words such as "may," "might," "will," "should," "expect," "plan," "anticipate," "believe," "estimate," "predict," "potential" or "continue," the negative of these terms and other comparable terminology. These statements are not historical facts but instead represent the Company's belief regarding future results, many of which, by their nature, are inherently uncertain and outside the Company's control. It is possible that actual results may differ, possibly materially, from those anticipated in these forward-looking statements. For a discussion of some of the risks and important factors that could affect future results, see the discussion in our Form 20F filed with the Securities and Exchange Commission under the caption "Risk Factors."

I bet we are at this meeting in paris

DRUGS IN DEVELOPMENT



EpiCept Announces Results of European Phase III Trial for LidoPAIN SP



ENGLEWOOD CLIFFS, N.J., Sept. 5, 2006 /PRNewswire-FirstCall/ -- EpiCept Corporation announced today that LidoPAIN(R) SP, a sterile prescription analgesic patch designed to provide sustained topical delivery of lidocaine to a post-surgical or post-traumatic sutured wound, did not meet its co-primary endpoints in a Phase III clinical trial in Europe.




The Phase III clinical trial was a randomized, double-blind, placebo-controlled trial of 440 patients who underwent hernia repair surgery. The trial results indicate that LidoPAIN SP did not achieve a statistically significant effect relative to placebo with respect to the primary endpoint of self-assessed pain intensity between 4 and 24 hours. In addition, a statistically significant effect was not achieved in the trial's co-primary endpoint of patient use of "rescue" medications, i.e. systemically-delivered analgesics used to alleviate pain.

The Company's initial analysis of the trial data indicates that the total amount of pain from 4-24 hours as measured by the area under the curve (AUC) had a p value of approximately 0.4; the co-primary endpoint of rescue medication use from hours 4-24 had a p value of approximately 0.09. Both treatment groups showed an analgesic effect with the greater analgesic response in the active group. The product was well tolerated in all treatment groups.

Jack Talley, President and Chief Executive Officer, stated, "We are obviously disappointed that LidoPAIN SP did not meet its co-primary endpoints, particularly in light of the positive results achieved by the product candidate in its Phase II trial. We will in particular be looking at changes which occurred in going from Phase II to Phase III. A thorough analysis of the trial results has been initiated and our findings will serve as the basis for our decision on next steps for this product candidate. As this analysis proceeds, we remain focused on continuing to advance our other late-stage pain and cancer product candidates in our pipeline, each of which target significant unmet medical needs. Notably, we remain on schedule to file our Marketing Authorization Application for Ceplene for Acute Myeloid Leukemia in Europe later this year, we are in the final stages of preparing our IND filing for EPC2407 a novel apoptosis inducer for certain types of cancer and we are continuing to scale up manufacturing for EpiCept NP-1 and LidoPAIN BP in anticipation of the initiation of pivotal trials."

About Ceplene(TM)

Ceplene is a registration-stage compound for the treatment of Acute Myeloid Leukemia (AML) as remission maintenance therapy. AML is the most common type of leukemia in adults, with an estimated 30,000 AML patients in the U.S. and an estimated 47,000 patients in the EU. There are currently no approved remission drug therapies for AML patients.

EpiCept is currently preparing a Marketing Authorization Application (MAA) in Europe for Ceplene. This MAA is expected to be filed in the fourth quarter of 2006. The basis of this application will be the results of a 320 patient Phase III clinical study, in which Ceplene met its primary endpoint of increased leukemia-free survival among AML patients in remission. Ceplene has been granted orphan drug status for the treatment of AML by the European Medicines Agency (EMEA).

About EpiCept(TM) NP-1

EpiCept NP-1 is a prescription topical analgesic cream designed to provide effective, long-term relief from the pain of peripheral neuropathies. Peripheral neuropathies are medical conditions caused by damage to the nerves in the peripheral nervous system. It is estimated that these conditions affect more than 15 million people in the U.S. alone and is associated with conditions that injure peripheral nerves, including herpes zoster, or shingles, diabetes, HIV and AIDS and other diseases. It can also be caused by trauma or may result from surgical procedures.

EpiCept has successfully completed Phase II clinical trials in the U.S. and Canada for EpiCept NP-1, which included 343 subjects. The Company is in the process of scaling up the production of NP-1 to prepare for the product candidate's Phase III clinical trials, which are scheduled to commence at the end of 2006. The initial planned indication for this product candidate is post-herpetic neuralgia, a specific type of peripheral neuropathy associated with shingles.

About LidoPAIN(R) BP

LidoPAIN BP is a prescription analgesic non-sterile patch designed to provide sustained topical delivery of lidocaine for the treatment of acute or recurrent lower back pain of moderate severity of less than three months duration. The LidoPAIN BP patch is intended to be applied once daily and can be worn for a continuous 24-hour period. The patch's adhesive is strong enough to permit a patient to move and conduct normal daily activities, but can be removed easily.

EpiCept has completed Phase II clinical trials in the U.S. for LidoPAIN BP. EpiCept is currently working towards scaling up production of this product candidate in order to commence Phase III clinical trials. These trials will be conducted in close consultation with Endo Pharmaceuticals, which is EpiCept's partner for the commercialization of LidoPAIN BP worldwide.

Conference Call

EpiCept will host a conference call to discuss the LidoPAIN SP trial results on September 6, 2006 at 8:30 AM EDT. To participate, please dial 888-243-6208 from the U.S. or Canada or 973-582-2869 from international locations (please reference access code 7834338).

About EpiCept Corporation

EpiCept is an emerging specialty pharmaceutical company focused on unmet needs in the treatment of pain and cancer. The Company has a staged portfolio of product candidates with several pain therapies in late-stage clinical trials, and a lead oncology compound (for AML) with demonstrated efficacy in a Phase III trial; the compound is intended for commercialization in Europe. EpiCept is based in New Jersey, and the Company's research and development team in San Diego is pursuing a drug discovery program focused on novel approaches to apoptosis.

If you are going to try so hard to ramp a share, ph, I suggest you read your own posts first.

No mention of EirX in the above post and it's a neagtive one - the drug didn't achieve what they hoped for, perfoming no better than the placebo.

starfrog is right there is NO mention of ERX IN the info above, there is a lot of similar research going on and SOME have no connection with ERX !

suggest you know what your talking about first starfrog

novel approaches to apoptosis

read the whole article

for new drug candidates with the potential to treat a range of cancers including
colorectal and breast tumours.
EiRx said it used its proprietary ALIBI and EnPAD technologies to discover
compounds with selective activity against cancer cells.
EiRx research director Finbarr Murphy said the lead compunds will be moved
into preclinical studies.
Chairman John Pool said: "This latest advance proves the potential of EiRx's
new EnPADTM technology to drive value creation through discovery of new drug
candidates, either to enlarge our in-house product pipeline or as a revenue
generating service offered to collaborative partners."
newsdesk@afxnews.com

potatohead - suggest you know what your talking about first starfrog

Well lets have a look at what I said, shall we:

1) No mention of EirX in the above post

Guess what? There isn't any mention (Point 1 to me I believe)

2) the drug didn't achieve what they hoped for, perfoming no better than the placebo.

And their wording: ".... The trial results indicate that LidoPAIN SP did not achieve a statistically significant effect relative to placebo...." (Point 2 to me as well)

So I suggest my post shows that I do know what I am talking about, wouldn't you think!

novel approaches to apoptosis

read the whole article

apoptosis apoptosis apoptosis apoptosis apoptosis apoptosis apoptosis

About Us .......................................................................................................................................... EiRx Therapeutics is a specialist provider of pre-clinical therapeutics to the pharmaceutical industry. Our unique scientific expertise and knowledge in the field of Apoptosis provide a sound base to discover and develop new medicines that will safely and selectively repair this natural process in disease. The potential benefits from these new medicines are enormous, since as many as 70% of all human disease have some defect in the control of Apoptosis.


EpiCept is an emerging specialty pharmaceutical company focused on unmet needs in the treatment of pain and cancer. The Company has a staged portfolio of product candidates with several pain therapies in late-stage clinical trials, and a lead oncology compound (for AML) with demonstrated efficacy in a Phase III trial; the compound is intended for commercialization in Europe. EpiCept is based in New Jersey, and the Company's research and development team in San Diego is pursuing a drug discovery program focused on novel approaches to apoptosis

potatohead - Youv'e completely lost the plot now.

Is EpiCept some strange anagram of EiRx?

There is no point in doing a google search on the word apoptosis and then cutting and pasting every article you find on the subject and sticking it here in the strange belief that it is somehow connected to this company. It isn't.

Rigel, Serono Enter $160M Aurora Kinase Inhibitor Deal



By Karen Pihl-Carey



Staff Writer
A preclinical program focused on Aurora kinase inhibitors brought Rigel Pharmaceuticals Inc. its fifth oncology deal, this one signed with Serono SA and worth up to $160 million.

Geneva-based Serono gains an exclusive license to develop and commercialize product candidates from the program everywhere, except Japan - although Serono could include that region at any time within two years. Rigel's lead candidate, R763, could move into clinical trials in 2006 if the company files an investigational new drug application as planned in December.

"For Rigel, this is a very important deal. It's our largest deal to date, and it's for a project that's the most advanced to date," said Raul Rodriguez, the South San Francisco-based company's executive vice president and chief operating officer. "This is a program that we think has tremendous potential and so we wanted to have a very aggressive partner. This amount of money is tremendous for us."

Terms call for Rigel to receive $25 million in initial payments - a $10 million license fee and a $15 million equity purchase at a premium to the market price that will give Serono less than a 3 percent stake in the company. Additional development and sales-based milestone payments for R763 bring the total value of the deal up to $160 million, not including royalties.

In early studies, R763 has been shown to inhibit proliferation and trigger apoptosis in several tumor cell lines, including those found in the cervix, lung, pancreas and prostate. With the agreement, Serono will cover all further development and commercialization costs of R763, as well as other product candidates that come out of the program.

"We're going to file the IND - Rigel is responsible for that effort in December of this year, which means in the first half of next year we could conceivably start trials," Rodriguez told BioWorld Today. He expects Serono will keep the same development timeline. "They wouldn't be paying this much money for a program if they were going to sit on it," he added. "They're going to be aggressive with it."

When Aurora kinase is overexpressed, it can cause cells to develop an abnormal number of chromosomes. At elevated levels, it is associated with cancers of the breast, bladder, colon, ovary, head and neck, and pancreas. By inhibiting it, a compound like R763 can arrest cell division and promote apoptosis. Rigel discovered R763 using its cell-based PAD assays applied to tumor cell lines.

"We are going to have the second most advanced Aurora kinase to go forward," Rodriguez said. "We have a product that is very potent and more selective, and ours is both oral and [intravenous], and the other one that's ahead of us is just I.V."

Vertex Pharmaceuticals Inc., of Cambridge, Mass., and partner Merck & Co. Inc., of Whitehouse Station, N.J., started a Phase I study of its Aurora kinase inhibitor VX-680 in January. The study is evaluating the product's safety and tolerability when administered in multiple cycles to patients with solid tumors refractory to prior chemotherapy treatment. Vertex and Merck signed their deal in June 2004. (See BioWorld Today, June 23, 2004.)

Also working in the Aurora kinase space are Sunesis Pharmaceuticals Inc., of South San Francisco, and Avalon Pharmaceuticals Inc., of Germantown, Md., to name a few.

While Serono is well known for its work in reproductive health, it has products positioned in the neurology, metabolism and growth and psoriasis markets. Only recently has it begun to establish new therapeutic areas of focus, including oncology. The company, which had worldwide revenues of $2.5 billion in 2004, currently has 30 ongoing development projects.

If R763 reaches the market, it could have blockbuster potential for Serono and Rigel, because it appears to work in so many different types of cancer.

"Taxotere and Taxol have been used in an equally broad number of tumor types as this," Rodriguez said, "and they have had well over $1 billion in sales."

In the pipeline, Rigel has three product development programs, including R763 for cancer, as well as R112 for allergy and asthma, and R406 for rheumatoid arthritis.

The Serono deal is its fifth collaboration in oncology, which is added to partnerships signed with New Brunswick, N.J.-based Johnson & Johnson on cell cycle inhibition; Basel, Switzerland-based Novartis AG on anti-angiogenesis targets; Tokyo-based Daiichi Pharmaceutical Co. Ltd. on a specific ubiquitin ligase target; and with Merck on various ubiquitin ligase targets. (See BioWorld Today, Jan. 15, 1999; Aug. 1, 2001; Aug. 13, 2002; and Nov. 16, 2004.)

Rigel also entered a deal with New York-based Pfizer Inc. earlier this year focused on preclinical work with IgE receptor inhibitors in respiratory mast cells to treat allergic asthma and other diseases. (See BioWorld Today, Jan. 21, 2005.)

Pfizer holds an option to license Rigel's Phase II rhinitis drug, R112. In August, the company enrolled the first patient in a 375-patient study comparing the compound with placebo and Beconase AQ (beclomethasone) nasal spray over a seven-day period. The trial should be complete in early December. Rigel also completed a Phase I study earlier this year of R788, its solid oral form of R406 (an oral liquid), for rheumatoid arthritis. A Phase I/II trial in RA patients is expected to begin in the first half of next year.

Cell death unnecessary for tumor suppression
Study shows p53's pathological responses to DNA damage are irrelevant to tumor suppression


6th September 2006 06:08 PM GMT]


--------------------------------------------------------------------------------

The unpleasant side effects of cancer treatments may not be necessary for successful tumor suppression, according to a paper in this week's Nature. Researchers report that widespread cell death caused by the tumor suppressor p53 in response to DNA damage is not required for p53 to block tumor formation. Instead, p53 stops tumor cells by responding specifically to oncogenic mutations.

"There's a growing understanding that p53 responds to many different types of stresses," said Laura Attardi of Stanford University in California, who was not involved in the study. "Some of those may be more central in tumorigenesis than DNA damage per se."

p53 induces apoptosis and cell-cycle arrest in cells with damaged genomes, and this response has been thought to underlie its ability to stop tumor formation, said the new study's senior author, Gerard Evan of the University of California, San Francisco (UCSF). These cellular pathologies also cause immune suppression, bone marrow depletion, hair loss, and other side effects of cancer therapies. "That has always been considered the inevitable downside of p53 acting as a tumor suppressor," Evans told The Scientist.

To see if this widespread cell death is necessary for tumor suppression, researchers led by Maria Christophorou, also of UCSF, examined DNA damage and tumor development in mice in which p53 can be reversibly turned on and off.

They first turned on p53 in mice for six days while exposing them to gamma irradiation. As expected, mice with functional p53 showed high levels of cell death in radiosensitive tissues, while mice without active p53 showed no such cell death. However, neither group of mice was protected against development of lymphoma.

"You'd think that if you have a situation where p53 is culling a large number of damaged cells, that that would make some difference (for subsequent tumor development), but it's not in this system," Attardi told The Scientist.

When the researchers turned off p53 during radiotherapy but turned it back on eight days later, the mice suffered no cell death or other cellular pathology but did show significant protection against lymphoma development - even though p53 did not kill off cells in response to DNA damage.

The results "clearly show you don't have to have p53 there when you damage the DNA to get tumor suppression," said Scott Lowe of Cold Spring Harbor Laboratory in New York, who was not involved in the study.

p53 signaling can be initiated not only by generalized DNA damage, but also by specific oncogenic mutations that disrupt the cell cycle. To see if this type of signaling could be responsible for p53's late protective effect against lymphoma development, the researchers examined the tumor suppressor p19ARF, which does not respond to DNA damage but activates p53 in response to aberrant cell proliferation. They found that p19ARF is necessary for p53 restoration to protect against radiation-induced lymphoma.

Instead of suppressing tumors by killing all damaged cells, p53 suppresses them by killing only those cells in which the damage has generated oncogenic mutations, according to Evan. P19ARF "activates p53 only in cells that really are in danger of giving you cancer," Evan said.

However, it's hard to say if "this will universally apply to every context or every tissue type," according to Attardi.

In humans, it's known that telomere shortening caused by DNA damage can induce p53 signaling, said Lowe. Laboratory mice do not suffer from telomere shortening, so the authors "couldn't assess whether that type of DNA damage could be relevant for activating p53's function as a tumor suppressor," he told The Scientist.

If p53's pathological response to DNA damage proves to be irrelevant to tumor formation in humans, blocking p53 activity during cancer therapies could alleviate unpleasant side effects, Evan suggested. "We could use drugs that will block that and yet we wouldn't suffer an increased cancer risk as a consequence as long as p53 is allowed to become active at some later point in time."