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

2 x 2 million at 0.2p just gone through!

A mixed bag today ! a good buying in price !

POT HEAD, WHERE ART THOU BULLSHIT NOW , PROBABLY DOWN THE TOILET ALONG WITH THE CRAP YOU TALK I HOPE
I AM STILL HOLDING 5M

JOINT VENTURE

stop the bullshit and keep holding!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Bought 1 mil today @.19 MM showed this as a sale shares up .03 whats going on?

halifax
Welcome aboard or was it a top up.

let me say this, cause we own 50% of all IPO relating to colon cancer out there, any news on google re colon cancer means the chance its relating to us is 2:1 odds.. bloody good odds if you ask me

http://www.wallstreetreporter.com/interview.php?id=18589&player=wma


if you listen we are intellectual property owners of 50% of all oncology targets which gives significant value. i.e. other pharmas are using our know how!!

and we must not forget this either

Re Gen insiders buy again

Vivian Lewis: "ReGen Therapeutics Plc has received notification from Tigran Kalaydjian that he is beneficially interested in 21,000,000 ordinary shares of the stock representing 3.03% of the current issued share capital.
This came a week after Dr P. Garrod, a non-executive director, that he has acquired 500,000 ordinary shares at 1.15 pence per share. Dr Garrod now holds and is beneficially interested in 66,750,000 ordinary shares representing 9.61% of the current issued share capital. The current price is right where he bought.
A British woman in a vegetative state will be given a sleeping pill which may "wake her up" against her family's wishes, reports the BBC. The 53-year-old, who has not been named, will be given zolpidem which early research has shown can bring people out of a vegetative state. It is being developed by ReGen Therapeutics and is in phase II trials.
After approval by the South African regulatory agency, ReGen Therapeutics Plc ReGen today announced that it has started dosing subjects in a clinical study designed to explore the effects of zolpidem in people who have suffered brain damage.
RGT-London AIM is up sharply, nearly 30%, not because of this development, but because of gossip about a European licensing deal before the end of the year. There is also talk of a takeover bid from an overseas drug company or of a joint venture with Eirx Therapeutics, also of London, traded as ERX. It is a drug discovery company seeking therapies for cancer, and recently announced results of preclinical in vivo animal studies, for its lead compound ERX3722 which was among a lead series of molecules identified from a screen of kinase inhibitors molecules which demonstrated selective killing of breast cancer cells over non-cancerous breast cells."
Editor's Note: Minutewoman.com, a web-based newsletter, provides exclusive monthly tips and analysis on selected international investments. Includes Email alerts to keep subscribers informed of newest briefs.

there is talk of news is out next week re joint venture

coming from you, I believe you !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! NOT

Leading UK scientist in Derry
Baroness Susan Greenfield was the guest of honour at a recent lunch hosted by the NWSTP at the University of Ulster's Magee Campus.

Speaking to an invited audience of senior academics, industrialists and other key stakeholders, Baroness Greenfield, who is regarded as one of the most influential voices in science policy in the UK, discussed her experience of the potential impact of Science and Technology on the regional economy.

In a short address, Baroness Greenfield covered various key and familiar issues including Intellectual Property, Technology Transfer, University Spin-Outs and the mis-match between the mindset of the Investor vs that of the Academic/Scientist.

Baroness Greenfield advocated the collaborative network approach taken by the NWSTP as key in terms of bringing together the various strands of opinion required in order that the impact of Science & Technology is maximized in a region.

She was speaking at the Magee campus during one of a number of engagements in the North West organised by the North West Science and Technology Partnership in collaboration with the University's Step Up programme. During these events, Invest NI were also acknowledged for their contributions through the Western Innovation Network programme managed by NORIBIC.
The Baroness stressed the need for urgent investment into biotechnology if cures are to be found for diseases such as cancer and Alzheimer's.

"Biotechnology is the very area we need to invest in if we are going to cure cancer, if we are going to cure Alzheimer's disease. We do need urgently investment in those areas," she said.

"My own view is that perhaps Government could help by subsidising or giving tax breaks to investors, if you can do it for the film industry, why not do it for the biotech industry.

"It is needed because we are getting increasingly convergent technologies.

"In the news recently, for example we've heard about artificial retina. One can imagine very soon, increasing technologies involving expertise in the biomedical sciences along with physical sciences, information technology and nanotechnology."

Baroness Greenfield also said Government should offer tax breaks or subsidies to investors in the biotechnology field.
Addressing an invited audience of academics and industry leaders, the Baroness stressed the importance of placing science at the centre of the new economy
"These technologies are going to lead to very exciting exploitation, very exciting possibilities for commerce."

Baroness Greenfield is currently a Professor of Pharmacology at Oxford University.

Life Peerage

She was granted a non-political Life Peerage in 2001 and awarded a CBE in the Millennium New Year's Honours List.
She has launched four academic start-up companies and is Director of the Royal Institution of Great Britain.
09 March 2007

From the other side a new patent has been applied for that looks good for ERX if bloody long.

and here is the new patent

http://v3.espacenet.com/textdoc?DB=EPODOC&IDX=WO2007017678&F=0

Description of WO2007017678



[0001] PYRAZOLO(1 ,5-A) PYRAMIDINE COMPOUNDS AND PHARMACEUTICAL COMPOSITIONS CONTAINING THEM

[0002] FIELD OF THE INVENTION

[0003] The present invention relates to certain pyrazolo[1 ,5-a]pyrimidine compounds, to processes for their preparation, compositions comprising them and methoda of using them. Novel screening methods are also provided.

[0004] BACKGROUND AND PRIOR ART

[0005] Apoptosis is a genetically regulated process of cell suicide that allows for the removal of unneeded, senescent or infected cells from the body while preserving the integrity and architecture of surrounding tissue. Whereas mitosis is responsible for the generation of new cells, apoptosis in contrast is responsible for removing the cells. It is this delicate balance of mitosis versus apoptosis that maintains tissue homeostasis.

[0006] Apoptotic pathways can be sub-divided into two categories, either the extrinsic apoptotic signals which are initiated on the outside of the cell by ligand engagement of cell surface receptors such as Fas and TNF receptors, and/ or the intrinsic pathways activated by signals emanating from cellular damage sensors (e.g. p53) or developmental cues. Although the pathways activated by extrinsic and intrinsic signals can overlap to some extent, receptor ligation (via an extrinsic signal) typically leads to recruitment of adapter proteins that promote caspase oligomerization and auto-processing

[0007] For example, following Fas ligand binding to the Fas receptor, the death signal is transmitted through conformational changes in preformed receptor clusters, resulting in the recruitment of the adaptor protein FADD (Fas-associated death-domain protein) through a DD-DD interaction. Once bound to Fas to form the death-inducing signalling complex, FADD then binds to the prodomain of caspase-8, which results in autoactivation of caspase-8 by proteolytic processing leading to cellular destruction {reviewed in Murphy et al Curr. Opin Pharm. 2003, 3:412-419).

[0008] In contrast, intrinsic signals usually operate by triggering the release of proteins from the mitochondria to the cytosol. Most notable among these is cytochrome c; binding of cytochrome c to a central apoptotic regulator, Apaf-1 , promotes oligomerization of Apaf-1 and, in a reaction requiring the ATPase activity of Apaf-1 , oligomerization and activation of caspase 9). Caspase 9 subsequently activates effector caspases such as 3, 6, and 7 and cellular destruction ensues (reviewed in Johnson & Jarvis 2004, Apoptosis.;9(4):423-7).

[0009] This targeted cell destruction is critical both in physiological contexts as well as pathological states. Apoptosis is the normal physiological response to many stimuli, including irreparable DNA damage. Various diseases evolve because of hyperactivation (neurodegenerative diseases, immunodeficiency, ischaemia-reperfusion injury) or suppression of programmed cell death (cancer, autoimmune disorders).

[0010] In cancer, the balance between mitosis and programmed cell death is disturbed, and defects in apoptotic pathways allow cells with genetic abnormalities to survive. The role of apoptosis in the genesis and progression of cancer has been well documented (e.g. Reed JC, 1999; J. Clin Oncol.17(9), 2941). Failure in normal apoptosis pathways contribute to carcinogenesis by creating a permissive environment for genetic instability and accumulation of gene mutations, promoting resistance to immune-based destruction, allowing disseverance of cell cycle checkpoints that would normally induce apoptosis, facilitating growth factor/hormone-independent cell survival, supporting anchorage- independent survival during metastasis, reducing dependence on oxygen and nutrients, and conferring resistance to cytotoxic anticancer drugs and radiation. Indeed, studies of colon specimens harvested at various points along the transformation of colorectal epithelium to carcinomas demonstrated a progressive inhibition of apoptosis (Bedi et al, 1995, Cancer Res. ;55(9):1811-6.)

[0011] COLON CANCER

[0012] Colorectal cancer is common in economically developed countries, particularly in Europe, North America and Australia and is the second leading causes of cancer-related deaths in the Western world. Every year, colorectal cancer is responsible for arr estimated 400,000 deaths worldwide. Approximately 60,000 people die from colorectal adenocarcinoma among the 150,000 new cases, which are diagnosed in Europe each year. A genetic contribution to colon cancer risk is suggested by two observations, namely a) an increased incidence of colorectal cancer among persons with a family history of colorectal cancer and b) families in which multiple family members are affected with colorectal cancer, in a pattern indicating autosomal dominant inheritence of cancer susceptibility (Burt et al 2004, Gastroenterology. 2004;127(2):444-51 ; Vasen et al 1996, Lancet. 17;348(9025):433-5). About 25% of patients with colorectal cancer have a family history of the disease while the remaining 75% of patients have sporadic disease, with no apparent evidence of inheriting the disease.

[0013] NATURAL HISTORY OF COLORECTAL CANCER

[0014] Colorectal tumours present with a broad spectrum of neoplasms, ranging from benign growths to invasive cancer and are predominantly epithelial in origin (i.e adenomas or adenocarcinomas). Pathologists have classified the lesion into three groups: nonneoplastic polyps, neoplastic polyps (adenomatous polyps, adenomas) and cancers.

[0015] Over 95% of colorectal cancers are carcinomas, most of which are adenocarcinomas. A personal/familial history of having colon adenomas places one at increased risk of developing colon cancer (Neale and Ritchie, in Herrera L, ed. Familial Adenomatous Polyposis. New York, NY; Alan R. Liss Inc., 1990 p61-66) suggesting that either the adenoma may reflect an innate or acquired tendency of the colon to form tumour or that adenomas might be the primary precursor lesion of the colon cancer. While there is no direct proof that the majority of colorectal cancers arise from adenomas, adenocarcinomas are generally considered to arise from adenomas because a) benign and malignant tissue occur within colorectal tumours (Perzin and Bridge 1981 , Cancer.48(3):799-819) and b) when patients with adenomas were followed for 20 years, the risk of cancer at the site of the adenoma was 25%, a rate much higher than the expected norm (Stryker et al 1987, Gastroenterology. 1987;93(5): 1009-13). In addition, removal of adenomatious polyps is associated with reduced colorectal cancer incidence (Muller and Sonnenberg 1995, Ann Intern Med. 15;123(12):904-10).

[0016] GENESIS OF COLON CANCER

[0017] The colon is organized into compartments of cells called crypts, where stem cells that reside near the bottom give rise to transit amplyifying cells that undergo five to seven additional divisions before they become terminally differentiated into one of four cell types, namely colonocytes, goblet cells, Paneth cells and enteroendocrine cells ( Brittan

[0018] & Wright 2004, Gut.;53(6):899-910). Three of the four cells types (exception being

[0019] Paneth cells) continue to migrate to the top of the crypt where they undergo apoptosis and are engulfed by stromal cells or are shed into the lumen. For tissue homeostasis to ensue, the birth rate of the colonic epithelial cells precisely equals ther rate of loss from the crypt apex. If birth/ loss ratio increases, a neoplasm occurs.

[0020] Since the differentiated epithelial cells have a fixed residency under normal conditions, it would appear that key to the genesis of colon cancer is that for cells to be able to accumulate mutations and form a polyp and early adenoma in this tissue, they have to become refractory to apoptosis. It is widely believed adenomas develop from normal stem cells through molecular abnormalities (Bach et al 2000, Carcinogenesis. 21(3):469- 76). However, a single random major deleterious molecular alteration is not sufficient to induce carcinogenesis. Indeed, even sustained expression of well known oncogenes, including SV-40 T antigen, human K-ras VaH 2 and a dominant negative mutant of human p53 alone or in combination do not lead to adenomas over a 9-12 month period (Kim et al 1993, J Cell Biol;123(4):877-93). One molecular alteration that seems pivotal to the genesis of colon cancer is the mutation of the APC protein such that approximately 85% of all colon cancers have this protein mutated. In addition, mutation of this gene seems to be one of the earliest events in the colorectal tumour progression pathway ( Kinzler & Vogelstein, 1998 in The Genetic Basis of Human Cancer (McGraw-Hill, Toronto). ). As such, the APC protein is viewed as a gatekeeper of colon cancer.

check out the new patent.. news imminent

GSK LOVES ERX

katcenka
Cheers plenty to read there that relates, that makes a change.

That's only part of the patent you should see the long winded stuff!

laurie
I like a long wind.

yes its talks about GSK, thats what i really like about it

http://www.madison.com/wsj/home/biz/index.php?ntid=122494&ntpid=2