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

Source: European Organisation for Research and Treatment of Cancer
Date: November 15, 2006
Post to: Slashdot, del.icio.us, Digg,
Furl, Netscape, Newsvine,
reddit, Yahoo! MyWeb

Enzyme Inhibitor Produces Stable Disease In Patients With Advanced Solid Cell Cancers
Preliminary trials of a MEK enzyme inhibitor have shown that it is capable of producing long-lasting stable disease in patients with advanced solid cancers. Tests showed that the drug inhibited key targets in the patients' tumours, and now it is being tested in phase II clinical trials.

Professor Alex Adjei told the EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Prague today (Wednesday 8 November) that the drug AZD6244 (ARRY-142886) inhibited MEK1/2 -- an enzyme that plays an important role in the Ras/Raf/MEK/ERK cell signalling pathway, which regulates cell proliferation and survival. Activation of this pathway has been implicated in a number of cancers, including lung, pancreatic, colon, melanoma and thyroid cancer.

"Laboratory studies have shown that AZD6244 has an effect on human tumours at nanomolar concentrations, and the first part of the phase I clinical trial has determined the maximum tolerated dose and the safety of the compound. Results from this second part of the trial demonstrate that a dose of 100mg of AZD6244 is well tolerated, produces a high incidence of long-lasting stable disease, and is associated with a profound inhibition of the cell signalling protein pERK and a reduction in cell proliferation -- which indicates that the drug is working against the tumours," said Prof Adjei, who was professor of oncology at the Mayo Clinic, Rochester, USA, before moving in October to be the senior vice-president for clinical research and chair of the Department of Medicine at the Roswell Park Cancer Institute, Buffalo, USA.

Prof Adjei and his colleagues at the Mayo Clinic, University of Colorado Health Sciences Center and Fox Chase Cancer Center recruited into the second part of the trial 34 patients with advanced cancers, including melanoma, breast, lung and colorectal cancers. Approximately 40% of the patients had melanoma. The researchers were particularly interested in this tumour type because a large proportion harbour B-Raf mutations, and tumours with these mutations may be highly sensitive to MEK inhibitors.

The patients were randomised to receive 100 or 200mg doses, twice a day for 28-day cycles. The larger dose proved to be too high for continuous dosing due to adverse side effects, but the smaller dose was well tolerated over a prolonged period.

The researchers tested biopsy tissue taken from the patients both before and after dosing. They found that the pERK protein was reduced by 77%. They also looked at another protein, Ki-67, which is used as a marker for cell proliferation. After dosing, there was a reduction in Ki-67 in nine out of 20 patients, and in five of those nine patients the reduction was at least 50% or more.

"We found that after 15 days of dosing, AZD6244 continued to inhibit pERK at times when concentrations of the drug in the blood were at their lowest levels between doses. At the lowest concentration, 400 nanograms of the compound per microlitre of plasma still corresponded to a 35-44% inhibition of pERK," said Prof Adjei.

Overall, 39 of 57 patients completed at least one cycle of treatment with AZD6244. After completion of the second cycle, 19 (49%) had stable disease, and nine of these patients (six melanoma, one each of breast cancer, non-small cell lung cancer and medullary thyroid cancer) remained stable for five or more months (range, 5-14+ months; median, 6 months). Two patients, one with thyroid cancer and the other with melanoma, continue to receive treatment with AZD6244 after one year. Sixteen of the 20 patients with melanoma completed at least one cycle of treatment. Twelve had stable disease after completion of cycle two, with stable disease persisting for at least five months in six patients (range, 5 - 13+ months; median, 6.5 months).

Prof Adjei said: "This drug shows initial promising results. It appears to be able to target cancers with over-activation of MEK and associated cell signalling pathways in an efficient manner. Furthermore, it is easy to give to patients as it comes in an oral formulation that can be swallowed. As a result, a number of phase II clinical trials have been initiated in patients with melanoma, pancreatic, lung and colon cancers."

New eRx certification promotes pharmacy interoperability
Healthcare IT News, ME - 13 Nov 2006
By Richard Pizzi, Associate Editor. ALEXANDRIA, VA SureScripts, the largest network provider of electronic prescribing services ...

PharmaMar presented data on two compounds at EORTC meeting
14 Nov 2006
Announces that it presented data on two of its compounds at the 18th EORTC (European Organisation for Research and Treatment of Cancer) meeting held in Prague, Czech Republic from 7-10 November 2006.

MADRID, Spain | Nov 14, 2006 | PharmaMar, the biopharmaceutical company specialising in cancer therapy, announces that it presented data on two of its compounds at the 18th EORTC (European Organisation for Research and Treatment of Cancer) meeting held in Prague, Czech Republic from 7-10 November 2006. Clinical data on Aplidin (plitidepsin) in paediatrics and pre-clinical data in neuroblastoma was presented. In addition, a poster presentation of pre-clinical data from PM 01120, a novel, synthetic compound related to variolins, was made. The key points from each of the presentations are set out below:

Oral presentation by B. Geoerger at the ITCC (Innovative Therapies for Children with Cancer) paediatric oncology session on 9 November 2006: Phase I-II clinical and pharmacokinetic study of plitidepsin in children with malignant tumours.

Data was presented from a study of 22 paediatric patients with confirmed malignant solid tumours. The key conclusions from the study were:

The observed toxicity and pharmacokinetic profiles in the paediatric population were similar to that seen in adults, with most toxicities being mild to moderate. Bone marrow toxicity is low.

Pharmacokinetic studies confirm a long half life and extensive tissue distribution with clearance increasing with age.

The recommended dose in paediatric patients is 5mg/m2, the same as in adults.

Preliminary anti-tumour activity was observed in neuroblastoma, medulloblastoma and pancreatoblastoma.

Poster: Antitumour activity of Aplidin in human neuroblastoma tumours H Sasak et al.

The objective of the study was to evaluate the in vitro and in vivo anti-tumour activity of Aplidin against a panel of paediatric human neuroblastoma cell lines and draw some preliminary conclusions about its activity in tumour-bearing animals. The key conclusions from the study were:

Aplidin produced strong potency (nanomolar or lower) in all pediatric neuroblastoma cell lines examined.

Aplidin at doses of 390, 375 and 325 g/kg was well tolerated on a qdx5 schedule. Aplidin at a dose of 450 g/kg was toxic on a qdx5 schedule.

Aplidin produced a 50% inhibition of tumor growth in SK-N-DZ xenografts when administered i.v. on a qdx5 schedule. Future plans include running multicycle treatment with Aplidin. Future plans include performing xenograft testing with other neuroblastoma cell lines using Aplidin dosed on a multicycle treatment schedule.



Poster: Pharmacokinetic evaluation of a novel anti-tumour agent, PM01120 by J Yin et al.

The objective of the study was to determine the pharmacokinetics of PM01120 in pre-clinical species. PM01120 is a novel synthetic anti-tumour agent related to variolins that were originally discovered in Antarctic sponge, Kirkpatrickia variolosa. PM01120 has demonstrated encouraging preclinical results against a panel of human leukaemic, ovarian and colon carcinoma cell lines, and multi-drug resistant cell lines, at very low concentrations.

Pharmacokinetic properties were established for PM01120 in pre-clinical species. PM01120 showed good oral bioavailability. Interspecies scaling projected a plasma clearance of 33.67mL/min/kg in humans.


About Aplidin (plitidepsin)
Aplidin is a synthetic cyclodepsipeptide originally isolated from the marine tunicate Aplidium albicans. The mechanism of action of Aplidin appears to involve oxidative mediated stress and is still under investigation. Aplidin induces rapid apoptosis and also inhibits the VEGF (Vascular Endothelial Growth Factor) autocrine loop, crucial in the vascularisation and growth of tumours. Human leukaemia and lymphoma tumour cell lines have been found to be particularly sensitive to Aplidin in models resistant to standard anticancer agents.

Aplidin has Orphan Drug designation from the EC and the FDA for Acute Lymphoblastic Leukaemia (ALL) and Multiple Myeloma (MM)


About PharmaMar
PharmaMar is the worlds leading biopharmaceutical company in advancing cancer care through the discovery and development of innovative marine-derived medicines. PharmaMar's clinical portfolio currently includes: Yondelis (co-developed with J&JPRD) in Phase III clinical trials; it was designated Orphan Drug status for soft tissue sarcomas and ovarian cancer by the European Commission (E.C.) and by the United States Food & Drug Administration (US FDA). Aplidin, in Phase II, designated Orphan Drug for acute lymphoblastic leukaemia and for multiple myeloma by the E.C. and by the FDA; Kahalalide F in Phase II, and Zalypsis and PM02734 in Phase I clinical trials.

PH-please would you mail me if you have time. Thanks MP

PH me to. Thanks!

New Vaccine Stimulates Colorectal Cancer Patient's Immune Systems To Fight Cancerous Cells


Colonoscopy in Colorectal-Cancer Screening for Detection of Advanced Neoplasia


'Virtual' Colonoscopy Considerably More Expensive


Grape Seed Extract Halts Cell Cycle, Checking Growth Of Colorectal Tumors In Mice


Virtual Colonoscopy Effective in Preventing Colorectal Cancer


A New Way To Treat Colon Cancer?



Colon Cancer Vaccine

British researchers have developed a vaccine that stimulates colorectal cancer patients' immune systems to fight cancerous cells.

In a clinical trial of 67 patients, researchers at the University of Nottingham observed that when the vaccines were administered before and after surgery to remove cancerous tumors, they helped stimulated immune cell production in up to 70 percent of patients. These results are published in the November 15 issue of Clinical Cancer Research.

"This is the first vaccine shown to stimulate TNF-alpha an immune-system protein that is very effective at killing cancer cells," said Lindy Durrant, senior author of the study and professor of cancer immunotherapy at the university.

The vaccine works by stimulating the patients' immune response to generate infection-fighting white blood cells called T cells, which in turn produce immune system proteins called cytokines that destroy cancer cells. The antibody contained in the vaccine, called 105AD7, was cloned from a patient who survived seven years with liver metastases from colorectal cancer, Durrant explained.

"This is very unusual as most patients die within one year of getting liver metastases," she said. "I thought if this antibody had helped this patient, if we could clone it, it might help others."

105AD7 is structurally similar to CD55, a protein that attaches to sugar molecules and is overexpressed in colorectal cancer cells, protecting them from attack by the body's immune system. While low levels of CD55 occur in all cells exposed to the immune system, increased expression of the protein has been observed in multiple types of tumors, including up to 80 percent of colorectal cancers.

During the trial - the largest to date looking at 105AD7 plus surgery -- 67 patients with colorectal cancer who were scheduled for surgery to remove their primary tumor were randomly assigned to receive either 100 micrograms of 105AD7 with a powder to help absorb the vaccine, 105AD7 along with BCG (a bacteria used to stimulate the immune system in cancer patients) during the first immunization and the powder in subsequent vaccinations, or no treatment.

The patients, who had varying degrees of disease, averaged age 66. Twenty-eight patients had colon cancer while in 39 patients the primary tumor was located in the rectum.

Patients were immunized before surgery on the day they were recruited for the study, and again two weeks later if surgery had not yet been performed. The vaccines were continued three, six and 12 weeks after surgery, and then at three monthly intervals up to a maximum of 24 months after surgery. Blood samples were collected from the patients during recruitment, at surgery, and at the time of the three-, six- and 12-week post-operative immunizations. Additional blood samples were acquired one month after each subsequent immunization.

Laboratory tests of the blood samples indicated that a T-cell response against the vaccine was recorded in the majority of patients. The responses tended to have two peaks: one following the start of the immunization schedule and another several months later, after additional immunizations. About 70 percent of patients produced both TNF-alpha and GM-CSF - a protein that stimulates white blood cell production in response to both the vaccine and to CD55.

"The immune responses to both the vaccine and CD55 were measurable, adding support to the use of CD55 as a target in cancer treatment," Durrant said.

Nineteen of the patients died during the follow-up period. Durrant and colleagues noted that the trial was not designed to study the effect of the vaccines on survival.

A bit of blue this morning at last !

2.3 million all buys!

yes thats cause we are on page 67 of the express amid takeover by a large US Pharma and tie up with RGT

and you all doubted me, its also rumoured the offer is at 4p a share.. so i think we can double that

4p CC What will do with all that money ! :)

I will tell ya later.. ;-) I know of another that will double in january.

: ))

Express reads:-

"Regen therapeutics was steady at 1.02p yesterday amid ongoing chatter that a European licensing deal was due in the next six weeks. There is also thought to be takeover interest from overseas pharma companies, and talk of a tie-up with Eirx Therapeutics, unchanged at .29p"

This could be very good news for both companies if there is foundation to these rumours. The Express were the ones who broke news of the US deal a couple of weeks beforehand.

Regen therapeutics is up 9.7% on the news.

That clip was taken from the dark side ?

It would be fantastic if, for once, a rumour proved to be true but I have faith in both companies to deliver what they set out to achieve, in time. I am more than happy to wait for either to be first with good news: the champagne is in the fridge, maturing nicely!
kim

Me to kim would be good :)

I'm happy. I have both ERX and RGT. Bit annoyed that I was going to top up RGT at the back end of October at 0.85p (Interims were very positive) - but forgot!!!!!!

Another Week, Another Takeover

Genentech (DNA) announced this morning the acquisition of Tanox (TNOX) for $919 mln in cash, a nice premium to yesterdays close.

One a week is all I ask.

Takeovers as a driver of the biotech sector valuation have been a theme of mine for some time long enough, in fact, that I sometimes feel like a stopped watch every time I write about it. I freely admit I didnt see pharmas acquisition spree in the private sector lasting as long as it did, nor did I believe that the disconnect between high private valuations and low public valuations would be so persistent. Now that the private sector is picked clean, its the turn of the public biotechs to see their valuations catch up.

I particularly pounded the table on biotech acquisitions around this time last year. The driver was new FASB acquisition accounting rules that create much less favorable accounting policies for drug company acquisitions of biotechs. In December 2005, however, FASB postponed the implementation date of the program. I opined at the time that this would push acquisitions into late 2006 and early 2007, presuming the expected effective date of the new rules to be year end 2007.

Were there now, so lets see if this early trickle of public acquisitions turns into a flood.

Revolving Door Biotech Portfolio Managers

The portfolio manager (PM) position at some funds is something of a revolving door particularly for sector PMs within larger macro funds. The door has been spinning particularly fast lately for biotech PMs. It has been a tough year for most biotech hedge funds as even those who are making money have been feeling a little overwhelmed by all the crosscurrents.

Short-siders are starting to get blind-sided by these acquisitions. Take these three recent acquisitions:



(I include the open call interest to reinforce what Ive written recently concerning short interest in the biotech sector specifically, it is very rare to find open options interest that correlates to the short interest number.)

Even if we assume all the open call interest was owned by those short the stock, which is unlikely in this sector, these deal announcements caused some migraines at a few funds. It's more likely the pain of the acquisition is magnified since biotech short sellers tend to be call sellers, too.

Any acquisition frenzy in a small sector like this feeds on itself. Speculators start moving in to see if they can pick the next takeout. Short sellers get nervous and start covering. Market caps rise, pushing prices paid higher. Rinse and repeat. It is a great deal of fun if youre long. Not so much if youre not.

When the process starts to really heat up, 100% acquisitions are replaced by big equity purchases at prices well above current market cap. For example, a company will come in and buy 19.9% of a target (keeping them off their balance sheets) for 3-5 times the current trading price of the target. Sometimes these deals come with a purchase option. Other times they dont. Youll see these deals about 3/4 of the way to the top of the cycle.

Whats at the top? The tippy-top is probably the second or third company that announces it is raising umpteen billion via a public offering to roll up small biotech companies. Theres a lot of money to be made when this nonsense starts happening, but your trigger finger needs to be pretty itchy.

Random Thoughts


It is not enough as an investor to simply acknowledge the Democrats' majority in Congress is likely to be bad for pharma companies. You have to (a) understand exactly how; and (b) figure out how to profit from it aside from the obvious shorting. The proposed rules will hit the blockbuster drugs sold through family physicians the hardest. Knowing pharma management realizes this and wont sit idly by while their sales and EPS plummet, you should start thinking about what drugs can replace the blockbusters. Drugs sold through specialists like cancer drugs and especially orphan indications are those most likely to be insulated from the worst of any regulations. Pharma has to go out and acquire these drugs. They dont own them now because the drugs dont fit their blockbuster mentality. Where do they find them? Small biotech companies.


The JP Morgan Healthcare Conference is Jan 8-11. Mark this down as it traditionally kicks off the biotech buying season. Remember the seasonal saw: Buy JP Morgan (JPM), sell ASCO.


In case my point in the blurb about Congress, pharma and blockbuster drugs was unclear, I dont think a Democratic majority in Congress is bad for biotech. Different? Yes. Bad for some companies? Particularly those intending to create mass-market lifestyle drugs. Net positive for the sector, though? I think so, but we wont know for certain until we see what the PDUFA-4 (Prescription Drug Fee User Act) proposals look like.


My firm lost the net connection in our office yesterday. We had a low-bandwidth wireless connection to a couple of laptops to keep us from going mad. It was disarmingly peaceful and productive in what has otherwise been a nutso week.


Its been interesting reading the comments on a piece I wrote saying Dendreons (DNDN) FDA panel early next year might be a pivot point for the sector. I opined a few weeks ago that a positive outcome to the panel might be as beneficial to the bulls as a negative panel outcome was to bears in the spring of 2004. This could be a considerable catalyst.


PDUFA-4? The regulatory framework of the FDA in terms of timing and user fees is memorialized in the Prescription Drug Fee User Act PDUFA. The first of these was signed last decade and they renew every three years. The reason I can be so confident that changes to the industry are coming is that PDUFA-3 expires September 30, 2007. It has to be renewed or else the FDA loses over 50% of its current budget.

Not too late StarFrog; if the rumours are right then both shares are dirt cheap at present!!
kim