driver
- 30 Mar 2006 17:03
StarFrog
- 13 Nov 2006 14:13
- 519 of 1180
What are you talking about 'TheMaster'. Just press your Trades button. People are selling (and buying, too). Got a short position out by any chance?
plm2349
- 13 Nov 2006 16:03
- 520 of 1180
will hit 0.4 before xmas
smiler o
- 13 Nov 2006 19:56
- 522 of 1180
Driver, back just in time , bad gales for scotland !!
potatohead
- 14 Nov 2006 13:52
- 523 of 1180
just been told by the company an analyst note will be out shortly..
;-)
looking foward to that
potatohead
- 15 Nov 2006 10:43
- 525 of 1180
showing blue, analyst report out any day
kimoldfield
- 15 Nov 2006 11:00
- 526 of 1180
Well, we can't argue with that PH!!
kim
potatohead
- 15 Nov 2006 11:45
- 527 of 1180
Mega deals are also being signed..
I think my 8p target may be a little underestimated
smiler o
- 15 Nov 2006 11:49
- 528 of 1180
Hello pot head you here again !! I hope your right Just get us to that 1p mark first please. :)
potatohead
- 15 Nov 2006 11:55
- 529 of 1180
Smiler, did you not get my email then, we are going to get over the coming weeks
an analyst update. Significant contracts.. I am told the company wont need to go to market for money anymore so must be mega mega bucks
if you want to see it mate, email me at *** and i will send it this evening
smiler o
- 15 Nov 2006 12:00
- 530 of 1180
POT HEAD YOU can e mail me just click on the yellow Sq next to my name
potatohead
- 15 Nov 2006 12:05
- 531 of 1180
ok you should have it now
potatohead
- 15 Nov 2006 12:06
- 532 of 1180
please dont post it on the BB
smiler o
- 15 Nov 2006 12:07
- 533 of 1180
No you can trust me PH ! :)
potatohead
- 15 Nov 2006 12:08
- 534 of 1180
tell me what ya think.. I like the info alot
potatohead
- 15 Nov 2006 12:53
- 535 of 1180
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."
potatohead
- 15 Nov 2006 14:28
- 536 of 1180
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 ...
potatohead
- 15 Nov 2006 14:48
- 537 of 1180
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.
moneyplus
- 15 Nov 2006 14:56
- 538 of 1180
PH-please would you mail me if you have time. Thanks MP