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Girl is cured of leukemia using stem cells from umbilical cord
Germany, November 30, 2010
Girl is cured of leukemia using stem cells from umbilical cord
Scientist Leipzig City confirmed ‘to have cured for the first time lymphoblastic leukemia with a transplant of stem cells from the umbilical cord of a nine years old girl. Life expectancy of the patient, who was suffering for three years, was reduced to three months before treatment was successful. ”
Vita 34, a company founded in 1997 by doctors at the eastern Germany city of Leipzig, announced this big news that was hopeful.
According to German experts, “the disease was diagnosed in the German girl at the age of three years and, after being treated with chemotherapy, it was found that their only chance of survival lay in a stem cell transplant.”
Dr. Eberhard Lampeter, medical director of Vita 34 explained that, “The life expectancy of the patient was reduced to three months without a stem cell therapy,” and said, “the cancer cells had already reached the brain.”
He also noted that “parents of the girl at the time of her birth decided to keep her umbilical cord, which was used to extract stem cells needed for her transplant.”
The professional said that “within 75 months from the intervention and now we can speak with certainty of a cure.”
According to the company, “A total of 15 children, including six with brain damage, could be treated so far with stem cells from their umbilical cords.”
Vita 34, also engaged in research on aging, multiplication and stem cell reprogramming and developing new stem cell based therapies to treat type 1 diabetes, brain damage and heart disease.
For the first time healing a leukemia by the own umbilical cord blood
Erstmals Heilung einer Leukämie durch das eigene Nabelschnurblut
VITA 34 Article
Nabelschnurblut kann Entzündungen dämpfen
Stammzellen aus dem Nabelschnurblut könnten in Zukunft Rheumatikern helfen. Davon sind chinesische Wissenschaftler überzeugt. Zumindest im Laborversuch an Zellproben und im Tierversuch an Mäusen haben die Stammzellen ihr heilendes Potenzial bewiesen. Die Forscher hatten Blut von Rheuma-Patienten mit fremden Stammzellen aus Nabelschnurblut vermischt. Diese undifferenzierten Zellen dämpften die Entzündung, indem sie bestimmte Zellen des Immunsystems, die bei dem Leiden überaktiv sind, sozusagen beruhigten. Im zweiten Teil der Untersuchung behandelten die chinesischen Forscher Mäuse, die an rheumaähnlichen Gelenkentzündungen litten, mit Stammzellen aus menschlichem Nabelschnurblut. Die Nager konnten sich darauf hin wieder besser bewegen. Die Entzündungen gingen messbar zurück. Im Gegensatz zu heute erhältlichen Medikamenten könne die Therapie mit den Stammzellen die Krankheit dauerhaft bessern, sagen die Forscher.
I have no US Stocks in my portfolio, because my english is not good enough.
I have selected some German biotechs for you with a time frame from 2-5 years with a big potential.
1. Paion
2. Morphosys
3. Evotec
4. 4SC AG
5. Wilex
6. VITA 34
This german biotech are highest risk with little money, some with a good potential by success. They are very risky, because they have no partner
1. Mologen
2. Cytotools
3. Biofrontera
All the others german biotechs are not so good. I have they only on the watchlist
Have a nice day
Erbse
Hi rikic,
yes thats my nickname at the Ariva Board.
What are your favourite stocks from the german biotechs. Can you order at FSE or XETRA.
I also look for biotechs with a time frame till 5-6 years or longer. In german there are not so many good biotechs with enough money. The most biotech stocks are very risky.
Hi rikic,
Paion presents at the Eigenkapitalforum in Frankfurt
PAION AG DE000A0B65S3 Dienstag, 23.11.2010 08:15-09:00 Room Madrid
I think, we get the Remimazolam results at this day or one day before, when the Conference started.
From where do you come. My home is also in Aachen, but i have nothing to do with Paion. Paion is one of mine favourite german biotech stock.
I hope you can understood my bad english. I learned my few Englisch words since about 45 years at my school time. But i never used my english and so it is very bad. I have a little Board withsome Paion facts.
German Erbses Paion Board
Have a nice day
Erbse
Hallo rikic
Schön, dass einer die Paion Aktie hier bekannt macht. Mein Englisch ist leider viel zu schlecht. Wenn es was wichtiges in Englisch zu kopieren gibt würde ich dir gerne helfen.
Grüße
Erbse
Hi gfp927 Propofol shortage
One of my german favourite PAION has a new CNS 7056 – anaesthetic/sedative in the development.
Here are some facts in german and english.
insert-text-here
insert-text-here
I have no Cortex shares since 1,5 years. It was a very nice time with you in the last 8 years. Please excuse my very bad english
Have a nice day
Erbse
Chronic treatment with AMPA receptor potentiator Org 26576 increases neuronal cell proliferation and survival in adult rodent hippocampus.
Su XW, Li XY, Banasr M, Koo JW, Shahid M, Henry B, Duman RS.
Division of Molecular Psychiatry, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, Yale University School of Medicine, New Haven, CT, 06508, USA.
RATIONALE: Currently available antidepressants upregulate hippocampal neurogenesis and prefrontal gliogenesis after chronic administration, which could block or reverse the effects of stress. Allosteric alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor potentiators (ARPs), which have novel targets compared to current antidepressants, have been shown to have antidepressant properties in neurogenic and behavioral models.
OBJECTIVES: This study analyzed the effect of the ARP Org 26576 on the proliferation, survival, and differentiation of neurons and glia in the hippocampus and prelimbic cortex of adult rats.
MATERIALS AND METHODS: Male Sprague-Dawley rats received acute (single day) or chronic (21 day) twice-daily intraperitoneal injections of Org 26576 (1-10 mg/kg). Bromodeoxyuridine (BrdU) immunohistochemistry was conducted 24 h or 28 days after the last drug injection for the analysis of cell proliferation or survival, respectively. Confocal immunofluorescence analysis was used to determine the phenotype of surviving cells.
RESULTS: Acute administration of Org 26576 did not increase neuronal cell proliferation. However, chronic administration of Org 26576 increased progenitor cell proliferation in dentate gyrus (~40%) and in prelimbic cortex (~35%) at the 10-mg/kg dosage. Cells born in response to chronic Org 26576 in dentate gyrus exhibited increased rates of survival (~30%) with the majority of surviving cells expressing a neuronal phenotype.
CONCLUSION: Findings suggest that Org 26576 may have antidepressant properties, which may be attributed, in part, to upregulation of hippocampal neurogenesis and prelimbic cell proliferation.
Have a nice day
Erbse
Positive AMPA receptor modulation rapidly stimulates BDNF release and increases dendritic mRNA translation.
Jourdi H, Hsu YT, Zhou M, Qin Q, Bi X, Baudry M.
Neurobiology, University of Southern California, Los Angeles, California 90089, USA.
Brain-derived neurotrophic factor (BDNF) stimulates local dendritic mRNA translation and is involved in formation and consolidation of memory. 2H,3H,6aH-pyrrolidino[2'',1''-3',2']1,3-oxazino[6',5'-5,4]-benzo[e]1,4-dioxan-10-one (CX614), one of the best-studied positive AMPA receptor modulators (also known as ampakines), increases BDNF mRNA and protein and facilitates long-term potentiation (LTP) induction. Several other ampakines also improve performance in various behavioral and learning tasks. Since local dendritic protein synthesis has been implicated in LTP stabilization and in memory consolidation, this study investigated whether CX614 could influence synaptic plasticity by upregulating dendritic protein translation. CX614 treatment of primary neuronal cultures and acute hippocampal slices rapidly activated the translation machinery and increased local dendritic protein synthesis. CX614-induced activation of translation was blocked by K252a [(9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester], CNQX, APV, and TTX, and was inhibited in the presence of an extracellular BDNF scavenger, TrkB-Fc. The acute effect of CX614 on translation was mediated by increased BDNF release as demonstrated with a BDNF scavenging assay using TrkB-Fc during CX614 treatment of cultured primary neurons and was blocked by nifedipine, ryanodine, and lack of extracellular Ca(2+) in acute hippocampal slices. Finally, CX614, like BDNF, rapidly increased dendritic translation of an exogenous translation reporter. Together, our results demonstrate that positive modulation of AMPA receptors rapidly stimulates dendritic translation, an effect mediated by BDNF secretion and TrkB receptor activation. They also suggest that increased BDNF secretion and stimulation of local protein synthesis contribute to the effects of ampakines on synaptic plasticity.
PMID: 19587275 [PubMed - in process
CX 717 Abstract from Greer John
Ampakine CX717 protects against fentanyl-induced respiratory depression and lethal apnea in rats.
Ren J, Ding X, Funk GD, Greer JJ.
Department of Physiology, Division of Neuroscience, University of Alberta, Edmonton, Alberta, Canada.
BACKGROUND: The use of fentanyl as a potent analgesic is contradicted by marked respiratory depression among a subpopulation of patients. The commonly used approach of reversing fentanyl-induced respiratory depression with mu-opiate receptor antagonists such as naloxone has the undesirable effect of blocking analgesia. Here, the authors report a clinically feasible pharmacological solution for countering fentanyl-induced respiratory depression via a mechanism that does not interfere with analgesia. Specifically, to determine if the ampakine CX717, which has been proven metabolically stable and safe for human use, can prevent and rescue from severe fentanyl-induced apnea. METHODS: Plethsymographic recordings were performed from young and adult rats. Varying doses of fentanyl were administered either intraperitoneally or intravenously to induce moderate to life-threatening apneas. CX717 was administered either before or after fentanyl administration. In addition, phrenic nerve recordings were performed from in situ working heart brainstem preparations from juvenile rats. RESULTS: Preadministration of CX717 markedly attenuated fentanyl-induced respiratory depression. Postadministration of CX717 rescued animals from a lethal dose of fentanyl. Significantly, CX717 countered fentanyl-induced depression of respiratory frequency without suppressing analgesia. The effective dose of CX717 was in the range deemed safe on the basis of clinical trials examining its efficacy for cognitive disorders. In situ, fentanyl-induced depression in respiratory frequency and amplitude was alleviated by CX717. CONCLUSIONS: CX717 is an agent that enhances the safety of using opiate drugs while preserving the analgesic effects. This advancement could significantly improve pain management in a variety of clinical settings.
OT PAION Hi bladerunner 1717
I have made a new board only with PAION news and articles. Some news are in english. I am sorry, some articles are in german.
When you are interested, here the link to the new PAION Board
http://www.ep.vm-elsig.de/yabb2/YaBB.pl
Discussion and pipeline from PAION
http://www.ep.vm-elsig.de/yabb2/YaBB.pl?num=1244886320
Have a nice day
Erbse
The AMPA receptor positive allosteric modulator, S18986, is neuroprotective against neonatal excitotoxic and inflammatory brain damage through BDNF synthesis.Destot-Wong KD, Liang K, Gupta SK, Favrais G, Schwendimann L, Pansiot J, Baud O, Spedding M, Lelièvre V, Mani S, Gressens P.
Inserm, U676, Paris, France; Université Paris 7, Faculté de Médecine Denis Diderot, Paris, France; PremUP, Paris, France.
Brain lesions induced in newborn mice by the glutamatergic agonists ibotenate (acting on NMDA and metabotropic receptors) or S-willardiine (acting on AMPA-kainate receptors) mimic some aspects of periventricular white matter lesions and neocortical grey matter damage observed in human neonates at risk for developing cerebral palsy. The neonatal mouse brain can be sensitized to excitotoxic damage by IL-1beta exposure similar to that observed in the human situation. Positive modulators of AMPA receptors have received increasing attention as potential neuroprotective agents in a number of neurodegenerative disorders of the adult. However whether they can also act as a neuroprotectant in neonatal brain damage has yet to be defined. Therefore the present study uses a well-defined rodent model of neonatal excitotoxic brain lesions to assess the neuroprotective effects of S18986, a positive allosteric modulator of AMPA receptors, as well as its mechanisms of action. In this model, S18986 provided a dose-dependent and long-lasting protection of developing white matter and cortical grey matter against an excitotoxic insult and also when this was combined with a sensitizing inflammatory insult. Neuroprotective effects of S18986 in cortical grey matter involved decreased necrotic and apoptotic cell death. S18986-induced neuroprotection against NMDA receptor-mediated brain lesions was blocked by inhibitors of ERK and PI3 kinase-Akt pathways. S18986 effects were abolished by a neutralizing anti-BDNF antibody and real-time PCR confirmed the stimulation by S18986 of BDNF production in the neonatal brain. The present study provides strong experimental support for the role of S18986 as a candidate molecule for therapy in cases of excitotoxic perinatal brain lesions and identifies BDNF as a key mediator of this S18986-mediated neuroprotection.
OT CNS 7056 PAION NeuroInv,
thanks for your answer. Here are some facts from a CNS 7056 study. I think they save a lot of time against Midazolam.
>>>Dose dependent sedation, with a rapid onset of effect, was observed after administration of CNS 7056 at doses of 0.05 mg/kg and higher. Doses of CNS 7056 (0.075 - 0.20 mg/kg) that induced peak sedation levels similar to or greater than those achieved with midazolam (0.075 mg/kg) showed a markedly shorter duration of sedative effect with recovery from sedation within approximately 10 minutes compared to approximately 40 minutes for midazolam. The peak sedative effect of CNS 7056 was reached within four minutes in these dose groups, with initial onset of sedation being observed after approximately one minute. For midazolam, the peak effect was reached after approximately 15 minutes. Duration and depth of sedation increased with higher doses of CNS 7056, while the recovery was still earlier as compared to midazolam. >>>
Have a nice day
Erbse
OT Neuroinv CNS 7056 PAION
Hi Dr Tracy, CNS 7056 is not only a new sedativum. It is better than Midazolam and is better than Propofol. Please look at the
CNS 7056 competitive advantage in the picture down of this side.
I think PAION have a very good chance with this compound.
Have a nice day
Erbse
Hi bladerunner OT CNS 7056
Hi bladerunner, OT
they have a good management. I will see them in two weeks at the annual general meeting. Yes they have a nice pipeline. This is worth a search.
They have the wrong strategy by the last desmoteplase stroke trial with the Penumbra Proof.
With the new strategy Vascular occlusion they have a good chance between 3 and 9 hours.
More Information about stroke and desmoteplase in english and german:
http://www.erbse.vm-elsig.de/form/base/YaBB.pl?num=1217124088;start=all
My favorit is CNS 7056 . They have a POC and the Phase 2 studie is ready at end of this year. They have a peak sales from 500 - 1000 Millions. With a cooparation Paion can get 20% til 25%. Now they have a marketcap from 25 Millions.
Here the information about CNS 7056
About CNS 7056
CNS 7056 is a new short-acting sedative and general anesthetic that acts on GABAA receptors. The substance was added to PAIONs portfolio by acquiring CeNeS who in turn had acquired the substance from GlaxoSmithKline. CNS 7056 is a water-soluble, rapid and short-acting GABAA receptor modulator interacting with the benzodiazepine site. The clinical proof of concept study, reported in January 2009, showed that, after intravenous administration, CNS 7056 rapidly induces sedation. Importantly the sedative effects rapidly disappear after cessation of administration. The rapid offset of effect of the compound is due to its metabolism by esterase enzymes that are widely distributed throughout the body. Therefore it is anticipated that CNS 7056 can be clinically developed as a sedative agent for day case procedures, the induction and maintenance of anesthesia and ICU sedation. PAION initiated partnering discussions in parallel to the ongoing Phase II in order to accelerate the further development of CNS 7056 for territories outside Japan, where the compound is partnered to Ono Pharmaceuticals.
Paion is listed at the OTC. but there are no trades. You can trade them at the german xetra or at the frankfurt stock exchange. It is better you take a limit.
Hope this helps
Erbse
Hi bladerunner 1717,
here the link to the PAION Homepage. You can switch it to english. They have a very nice homepage. Some information about PAION in my board is also in english.
http://www.paion.de/
Cash about 33 Millions € at end of march this year
Cashburn about 12-13 Millions € a year.
Marketcap. about 25,8 Millions today
Number of shares about 24,6 Millions
They have to outlicense the pipeline, because they have not enough cash. They have 3 compounds from its own and 3 compounds from the CENES takeover from the last year. You could read it all from the PAION Homepage.
Investors
Report&Presentations
Annual Report 2008
Very interesting is the presentation from the same page
Current corporate presentation (presented at conference call "Financial results 2008")
News in german and english
http://www.finanznachrichten.de/nachrichten-aktien/paion.asp
My english is very bad. Please excuse my mistakes.
Have nice day
Erbse
Hi gfp927z, here the link of the German Cortex Board.
http://www.erbse.vm-elsig.de/form/base/YaBB.pl
I am not in TTNP. I am not in COR. My last position in biotech is PAION. It is a Biotech from my hometown Aachen in Germany. You could also find the facts about PAION in the Cortex Board. I think it is better than Cortex.
Have a nice day
Erbse
OT Targacept Announces Positive Top-Line Results from Phase II Study of AZD3480 in Adult ADHD
Winston-Salem, NC
May 11, 2009
Targacept, Inc. (NASDAQ: TRGT) today announced preliminary results showing that AZD3480 (TC-1734) met the primary outcome measure in a Phase II clinical study in adults with attention deficit/hyperactivity disorder (ADHD).
In the study, adult subjects received in random order daily doses of 5mg of AZD3480, 50mg of AZD3480 and placebo, each for two weeks with the dosing periods separated by a three-week washout period. At 50mg AZD3480, subjects showed statistically significant (p < .01) improvement in symptoms of ADHD as measured by the study’s primary outcome measure, total symptom score on the Conners Adult ADHD Rating Scale – Investigator Rating (CAARS-INV). Data from the study on CAARS-INV are shown in the table below.
Completed Subjects Pre-Treatment Mean (Standard Deviation) Post-Treatment Mean (Standard Deviation) Mean Change
(Standard Deviation)
placebo 24 37.7 (5.45) 36.9 (5.20) 0.8 (5.33)
5mg AZD3480
23 39.6 (5.36) 34.9 (5.24) 4.7 (5.30)
50mg AZD3480 24 40.3 (5.40) 33.1 (5.34) 7.2 (5.37)
Statistically significant results were also achieved at 50mg AZD3480 on a number of secondary outcome measures in the study, including Stop Signal Reaction Time, a computerized assessment of behavioral inhibition, which is a core cognitive deficit of ADHD.
AZD3480 was well tolerated in the study, and there were no serious adverse events.
“In this study AZD3480 positively affected the core symptoms of adult ADHD patients. The results showed a consistent effect between improvements in clinical symptoms and a core cognitive deficit. Additionally, we saw improvement after just one week of treatment with the 50mg dose of AZD3480 and then continued improvement at the end of the second week,” commented Paul A. Newhouse, M.D., Professor of Psychiatry and Director, Clinical Neuroscience Research Unit and Brain Imaging Program, University of Vermont College of Medicine, and the principal investigator for the study.
“These results further our belief in AZD3480’s potential to benefit patients and reinforce our longstanding commitment to the neuronal nicotinic receptor mechanism. AZD3480 has now been studied in over 1,350 subjects providing us and AstraZeneca with substantial data,” said J. Donald deBethizy, Ph.D., President and Chief Executive Officer of Targacept.
“We are encouraged by the preliminary results of the study presented to us. There is a compelling need to develop novel, well-tolerated, non-stimulant medicines to meet the needs of patients with ADHD,” said Bob Holland, Vice President Neuroscience and Head of the Neuroscience Therapy Area, AstraZeneca. “We look forward to completing a full analysis of the data set and then making our decisions around the future development of this compound.”
Next Steps
Analyses of the full dataset from the study remain ongoing. AstraZeneca and Targacept plan to present and publish more detailed results from the study at a future scientific meeting.
AstraZeneca is expected to determine whether to conduct further development of AZD3480 in ADHD and/or Alzheimer's disease in the second quarter of 2009.
Study Design
Double blind, placebo controlled, crossover study conducted at Fletcher Allen Health Care, an affiliate of the University of Vermont College of Medicine.
Subjects were between the ages of 18 and 65, male and female, non-smokers, diagnosed with ADHD based on DSM-IV criteria and had a baseline score of at least 4 on the Clinical Global Impression – Severity scale.
Efficacy dataset included 24 completed subjects.
Each subject received in random order 5mg of AZD3480, 50mg of AZD3480 and placebo, in each case daily for two weeks, with the dosing periods separated by a three-week washout period designed to minimize carryover effects. As a result, each subject served as his or her own control.
The primary outcome measure was the change in total symptom score on the Conners Adult ADHD Rating Scale – Investigator Rating (CAARS-INV) following two weeks dosing with AZD3480 as compared to two weeks dosing with placebo.
http://www.targacept.com/wt/page/pr_1242008964
PAION’s Novel Sedative/Anaesthetic CNS 7056 Meets Target Profile in Human Proof of Concept Study
Sedation with fast and predictable on- as well as offset
Favourable safety profile
New Phase I/II studies in preparation
The biopharmaceutical company PAION AG (News/Aktienkurs) (ISIN DE000A0B65S3; Frankfurt Stock Exchange, Prime Standard: PA8; London AIM: PAI) today reports the first human data of its intravenous sedative/anaesthetic CNS 7056. The Phase I proof of concept study compared intravenous CNS 7056 to placebo and a standard dose of midazolam, the current gold standard for procedural sedation. The anticipated favourable profile was observed and no safety issues were raised. Volunteers treated with increasing doses of CNS 7056 were successfully sedated at the higher dose cohorts as expected and recovered to full consciousness rapidly.
A total of 81 subjects were enrolled in the double-blind placebo- and midazolam- controlled Phase I study. The study was designed to explore the safety, tolerability and pharmacokinetics of single ascending doses of CNS 7056 in healthy volunteers. Efficacy was ascertained by assessing the sedation of the volunteers by standardized methods. Midazolam-treated volunteers were included to allow an initial assessment of the comparative efficacy and safety profile of CNS 7056. The stopping criterion for the study was pre-determined as more than 50% of the volunteers reaching loss of consciousness for more than 5 minutes. In the 9th out of 10 planned doses this criterion was met. No serious adverse events occurred, even at doses that induced unconsciousness.
Dose dependent sedation, with a rapid onset of effect, was observed after administration of CNS 7056 at doses of 0.05 mg/kg and higher. Doses of CNS 7056 (0.075 - 0.20 mg/kg) that induced peak sedation levels similar to or greater than those achieved with midazolam (0.075 mg/kg) showed a markedly shorter duration of sedative effect with recovery from sedation within approximately 10 minutes compared to approximately 40 minutes for midazolam. The peak sedative effect of CNS 7056 was reached within four minutes in these dose groups, with initial onset of sedation being observed after approximately one minute. For midazolam, the peak effect was reached after approximately 15 minutes. Duration and depth of sedation increased with higher doses of CNS 7056, while the recovery was still earlier as compared to midazolam.
The company now plans one study with healthy volunteers in colonoscopies and one study with patients undergoing upper gastrointestinal endoscopies. Both studies are expected to start no later than Q3 2009.
CNS 7056 is an ester and pre-clinical studies showed that it is rapidly hydrolysed by tissue esterases to an inactive metabolite. This mechanism of deactivation should result in a more predictable onset and offset profile compared to that seen with drugs that are predominantly metabolized by the liver and, secondly, a lower risk of pharmacokinetic drug interactions. Pharmacokinetic analysis from the current Phase I study confirmed that CNS 7056 was rapidly converted to its inactive metabolite in man. The plasma clearance of CNS 7056 was approximately three times more rapid than the clearance of midazolam. The pharmacokinetic profile of CNS 7056 was linear within the dose range examined.
PAION will now progress to the next stage of development and start seeking a partner for territories outside Japan in parallel to the commencement of Phase II. In Japan, CNS 7056 is partnered with Ono Pharmaceuticals.
Wolfgang Söhngen, CEO of PAION commented: ”The positive data meet our expectations. We are positive that CNS 7056 could be a valuable alternative for procedural sedation by avoiding the potential for prolonged or overly deep sedation thus potentially reducing the intensity of supervision needed. We will seek ways to explore its potential also in other indications. It was especially re-assuring to see that sedation, to the level of unconsciousness, could be achieved without safety concerns. PAION’s management and project team are proud to see that these results confirm our high expectations for the potential of this compound, which was in the pre-clinical development phase when we completed the CeNeS acquisition last summer.”
Note: An updated company presentation including the new data on CNS 7056 will be available on www.paion.com starting Monday, 12 January 2009.
PAION complete Enrolment of Phase IIa Study with CNS 5161
PAION and ERGOMED Complete Enrolment of Phase IIa Study with CNS 5161 in Opioid-Refractory Cancer Pain
The biopharmaceutical company PAION AG (News/Aktienkurs) (ISIN DE000A0B65S3; Frankfurt Stock Exchange, Prime Standard: PA8; London AIM: PAI) and ERGOMED Clinical Research Limited today announce the completion of an open-label, single-centre Phase IIa study with PAION's intravenous NMDA receptor antagonist CNS 5161. The study has been completed by PAION and ERGOMED under a Revenue Sharing and Co-Development Agreement signed in July 2006.
In the study, a total of 24 patients with opioid-refractory cancer pain were recruited into six ascending dose groups. Patients received six doses of the compound over a 24 hour period. The goals of the study were to determine the maximum tolerated dose and to assess efficacy and pharmacokinetic parameters of CNS 5161. Increasing analgesic effects were detected with increasing doses. Significant side-effects or psychomimetic effects, often associated to the NMDA receptor antagonist compound class, have not been observed. The company expects full results of the study at the end of the first quarter 2009.
CNS 5161 is an NMDA receptor antagonist for the treatment of neuropathic pain and late-stage cancer pain. Prior to the now completed Phase IIa study, which was the first multiple administration study of CNS 5161, proof of concept clinical trials have been conducted to profile the compound as a novel therapy to treat neuropathic pain. Two Phase I studies have demonstrated the safety and tolerability of CNS 5161 as well as showing evidence of analgesia in a pain model. In addition, two small Phase II studies have been completed giving single intravenous infusions of CNS 5161 to patients with long standing intractable neuropathic pain. Both studies reported analgesic effects of CNS 5161 without psychomimetic effects.
Dr Wolfgang Söhngen, CEO of PAION commented: ”It is very encouraging that despite the small study size, analgesic effects were observed throughout all patient groups without significant side-effects. Together with ERGOMED, we are going to decide on the next steps once the full results become available. Larger studies are required to fully prove the promising profile demonstrated by this study and it is likely that partners will be sought to undertake these studies.”
Dr Miroslav Reljanovic, CEO of ERGOMED added: ”We are very pleased with the results from this study with CNS 5161 and we look forward to working with PAION to realise its full value.”
Pain is an inevitable consequence of most solid cancers. It has been estimated that nearly three million patients in the seven major markets will require treatment for cancer pain annually and that more than 70 % of late stage cancer patients suffer from moderate to severe pain (Source Apex Healthcare). Opioids are commonly used for managing moderate to severe cancer pain, but it has been estimated that around 20 % of patients will experience opioid-refractory pain that has to be treated using alternative therapies.
Homepage PAION: http://www.paion.de/
Have a nice day
Erbse
Yes he did.
Here a link to the old Deadwyler abstracts
http://www.erbse.vm-elsig.de/form/base/YaBB.pl?num=1127052657/1#1
Have a nice day
Erbse
Mechanisms underlying cognitive enhancement and reversal of cognitive deficits in nonhuman primates by the ampakine CX717.
Hampson RE, España RA, Rogers GA, Porrino LJ, Deadwyler SA.
Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC, 27157-1083, USA.
RATIONALE: Performance of cognitive tasks in nonhuman primates (NHPs) requires specific brain regions to make decisions under different degrees of difficulty or "cognitive load." OBJECTIVE: Local cerebral metabolic activity ([(18)F]FDG PET imaging) in dorsolateral prefrontal cortex (DLPFC), medial temporal lobe (MTL), and dorsal striatum (DStr) is examined in NHPs performing a delayed-match-to-sample (DMS) task with variable degrees of cognitive load.
MATERIALS AND METHODS: Correlations between cognitive load and degree of brain metabolic activity were obtained with respect to the influence of the ampakine CX717 (Cortex Pharmaceuticals), using brain imaging and recordings of neuronal activity in NHPs and measures of intracellular calcium release in rat hippocampal slices.
RESULTS: Activation of DLPFC, MTL, and DStr reflected changes in performance related to cognitive load within the DMS task and were engaged primarily on high load trials. Similar increased activation patterns and improved performance were also observed following administration of CX717. Sleep deprivation in NHPs produced impaired performance and reductions in brain activation which was reversed by CX717. One potential basis for this facilitation of cognition by CX717 was increased firing of task-specific hippocampal cells. Synaptic mechanisms affected by CX717 were examined in rat hippocampal slices which showed that N-methyl-D: -aspartic acid-mediated release of intracellular calcium was reduced in slices from sleep-deprived rats and reversed by application of CX717 to the bathing medium.
CONCLUSIONS: The findings provide insight into how cognition is enhanced by CX717 in terms of brain, and underlying neural, processes that are activated on high vs. low cognitive load trials.
The Christmas wishes of a Cortex shareholder
Have a nice day
Erbse
Is the studie ready ?
Trial to Determine the Maximum Tolerated Dose (MTD,) Based on Safety and Tolerability, of Org 26576 in Patients With Major Depressive Disorder (174001)
This study is ongoing, but not recruiting participants.
http://www.clinicaltrials.gov/ct2/show/NCT00610649?term=26576&rank=1
Have a nice day
Erbse
(PAION) Lundbeck started new Desmoteplase Study
Stroke - cerebral thrombosis
Before the end of 2008, Lundbeck expects to initiate a new Phase III clinical programme with desmoteplase for the treatment of patients suffering from stroke. After consultations with the US health authorities (FDA), the programme will consist of two Phase III placebo-controlled studies, each enrolling about 320 patients with the aim of measuring efficacy of one dosage of desmoteplase (90microgram/kg) administered in a window of between 3 and 9 hours after the stroke occurred. About 80% of patients suffering from a stroke are not ready for treatment until after more than 3 hours after they were hit by the stroke. There is currently no approved medical treatment to be initiated more than three hours after the stroke occurred. The efficacy of desmoteplase will be assessed after 90 days.
Source: http://www.lundbeck.com/investor/releases/ReleaseDetails/Release_1268934_EN.asp
New Ampakine Patent from John Greer
METHOD OF INHIBITION OF RESPIRATORY DEPRESSION USING POSITIVE ALLOSTERIC AMPA RECEPTOR MODULATORS
Abstract of US 2008261962 (A1)
The invention is directed to a method for alleviating respiratory depression in a subject as a result of disease of pharmacological agents such as opiates, opioids or barbiturates. The invention also discloses pharmaceutical compositions for use with the method, the composition containing in combination, an analgesic, anaesthetic, or a sedative and a positive allosteric AMPA receptor modulator in an amount sufficient to reduce or inhibit respiratory depression caused by the analgesic, anaesthetic, or sedative.
Source: http://v3.espacenet.com/publicationDetails/biblio?KC=A1&date=20081023&NR=2008261962A1&DB=EPODOC&locale=en_EP&CC=US&FT=D
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Erbse
A Follow up Safety Study of Patients Who Participated in Previous Studies of the Drug Org 24448 (Study P05719)
This study is enrolling participants by invitation only.
http://www.clinicaltrials.gov/ct2/show/NCT00780585?term=24448&rank=2
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Erbse
OT Hello scstocks. Here another animated gif.
It is a hobby from a boyfriend of mine. I give him some Euros and he make the animated gif from Cortex and PAION.
Have a nice Helloween
Erbse
Happy Halloween all you Cortex Freaks
New Patent for Ampakines
TREATMENT OF FEMALE SEXUAL DYSFUNCTION BY COMPOUNDS THAT POSITIVELY MODULATE AMPA-TYPE GLUTAMATE RECEPTORS
http://v3.espacenet.com/textdoc?DB=EPODOC&IDX=WO2008118644&F=0&QPN=WO2008118644
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Erbse
Ampakine Abstracts Neuroscience Meeting 2008
Effects of Ampakines on hippocampal CA1 pyramidal neurons
Ampakines enhance axonal outgrowth by cortical neurons
Inhibition of XII inspiratory output by μ-opioid receptors is presynaptic and alleviated by ampakines
A nootropic drug Ampakine(CX-717)potently modulates synaptic AMPA receptor single channel properties
http://www.erbse.vm-elsig.de/form/base/YaBB.pl?num=1221912222
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Erbse
Evaluation of the pro-cognitive effects of the AMPA receptor positive modulator, 5-(1-piperidinylcarbonyl)-2,1,3-benzoxadiazole (CX691), in the rat.
Psychopharmacology (Berl). 2008 Sep 16. [Epub ahead of print]
PMID: 18795266 [PubMed - as supplied by publisher]
GlaxoSmithKline tested CX691
Evaluation of the pro-cognitive effects of the AMPA receptor positive modulator, 5-(1-piperidinylcarbonyl)-2,1,3-benzoxadiazole (CX691), in the rat.
Woolley ML, Waters KA, Gartlon JE, Lacroix LP, Jennings C, Shaughnessy F, Ong A, Pemberton DJ, Harries MH, Southam E, Jones DN, Dawson LA.
Neurosciences Centre of Excellence for Drug Discovery, GlaxoSmithKline plc, New Frontiers Science Park, Third Avenue, Harlow, Essex, CM19 5AW, UK, marie.2.woolley-roberts@gsk.com.
RATIONALE: Positive allosteric modulators of the glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoazolepropionic acid (AMPA) receptor do not stimulate AMPA receptors directly but delay deactivation of the receptor and/or slow its desensitisation. This results in increased synaptic responses and enhanced long-term potentiation. Thus, it has been suggested that such compounds may have utility for the treatment of cognitive impairment. OBJECTIVES: The objective of the study was to investigate the effect of an AMPA positive modulator, CX691, (1) in three rodent models of learning and memory, (2) on neurochemistry in the dorsal hippocampus and medial prefrontal cortex following acute administration, and (3) on brain-derived neurotrophic factor (BDNF) messenger RNA (mRNA) expression in the rat hippocampus following acute and sub-chronic administration. RESULTS: CX691 attenuated a scopolamine-induced impairment of cued fear conditioning following acute administration (0.1 mg/kg p.o.) and a temporally induced deficit in novel object recognition following both acute (0.1 and 1.0 mg/kg p.o.) and sub-chronic (bi-daily for 7 days) administration (0.01, 0.03, 0.1 mg/kg p.o.). It also improved attentional set-shifting following sub-chronic administration (0.3 mg/kg p.o.). Acute CX691 (0.1, 0.3 and 1.0 mg/kg, p.o.) increased extracellular levels of acetylcholine in the dorsal hippocampus and medial prefrontal cortex and dopamine in the medial prefrontal cortex. Sub-chronic administration of CX691 (0.1 mg/kg, p.o.) elevated BDNF mRNA expression in both the whole and CA(1) sub-region of the hippocampus (P < 0.05). CONCLUSIONS: Collectively, these data support the pro-cognitive activity reported for AMPA receptor positive modulators and suggest that these compounds may be of benefit in treating disorders characterised by cognitive deficits such as Alzheimer's disease and schizophrenia.
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Erbse
Targacept: Commentary NeuroInvestor
(9/16/08 comment on Phase IIb Alzheimer's data)
Targacept/AstraZeneca's TC-1734/AZD-3480 underwhelmed with its Phase IIb Alzheimer's results, topline data released by partner AstraZeneca. It did not definitively fail, even though it missed its primary endpoint, but even when looking at the silver lining, it does appear expectations for this drug in dementia will have to be ramped down. Here are some of the interesting findings and our conjectures:
1) That confounding placebo effect. The placebo group did not show the modest decline one would expect over just three months, indeed they improved. And of course, the safety/tolerability profile of the placebo was outstanding. In retrospect, AZ may/should kick themselves for not running a six month trial, where such an effect is likely to diminish.
2) The benefit of AZD3480 did not outshine Aricept in any consistent way, though it did outperform Aricept on the ADS-CGIC. That is a caregiver/prescriber assessment of patient outcome, which to some degree represents a shot at capturing real-life functional gains that do not translate well into cognitive test scores, but this kind of data is also more subjective and 'squishy'.
3) The report of benefit on the blunt-instrument MMSE is not entirely reassuring, we would have hoped to see some trend on the more detailed CDR, and perhaps something will yet come from more detailed analysis of the several domains assessed.
4) Aricept did not perform any better, and indeed was worse on the ADS-CGIC. It is a reminder that even this lucrative gold standard drug doesn't present all that high a hurdle to match, and matching it is a consolation prize at best.
5) The patient population in this large (567 patients were dosed, at 84 sites!) trial was from Europe and Canada. We will be curious to see what proportion was enrolled in Eastern Europe, where the quality control and experience that can be assumed in clinical trial execution is not as assured, but rapid enrollment is. Just as we have some qualms about Medivation's reliance upon 181 Russian patients, we wonder if there was any divergence associated with those trial sites.
6) There is a modest signal of effect here, but based on what is known thus far, one would have to project a drug which is as effective, but probably not superior to, Aricept in terms of efficacy, but has better tolerability. Whether that will be enough to persuade AstraZeneca to go into Phase III (which would have to be at least six months of treatment) remains to be seen.
7) This raises the stakes on the schizophreniform cognition Phase IIb results, which will be out in December, the same month that AstraZeneca has to decide whether or not they are going to go into Phase III for AD or schizophrenia, and pay the requisite milestone to Targacept. ADHD data will be out in early 2009, but AZ will have to make its decision before then.
8) While comparing studies is a dicey proposition, it is worth noting that Memory Pharma's nicotinic alpha 7 drug (MEM3454), which has a different target than AZD3840, which is an alpha4beta2 modulator, produced a statistically significant effect on the CDR in just eight weeks. Interestingly, both drugs showed an inverted-U response curve, with the mid-dose performing best. This leaves open the question of which NNR target is optimal for AD, and what about the pharmacokinetics of these drug/receptor interactions lead to this dimunition of effect with higher doses.
Ich finde das lustig. Man sollte das Leben mit Humor nehmen. Es war der Google Translator
Schönen Tag noch
Erbse
We have the whole year vacation in Germany. Then we drink a lot of beer. If we do not have holidays, then we have Christmas. This can take a very long time with the results.
Greetings
Erbse
Hi RBlatch. Here a screenshot from the Cortex homepage. My slide from the Cortex Development Pipeline is only for people.
I think CX 701 for animals is active, but i have only the information from the homepage.
Erbse