Human Genome Sciences Inc. (HGSI) (1 Viewer)
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PiggiNO
Nuovo forumer
Sono da tenere o no e fino a che tp.. secondo te ovviamente.. ciao e grazie
coxy
coxy
1. HGSI è solo il Benlista + antiantrace ed Albuferon? No.
2. Il Benlista è solo possibile principio terapeutico anti-Lupus (SLE) o è utilizzabile in altre malattie autoimmuni o con una componente auto-immune? Questo forse lo sanno solo alla GSK. SE sì, la capitalizzazione attuale dovrebbe essere più che giustificata.
1.1 HGSI ha altri principi terapeutici uno sviluppato dalla GSK ed uno sviluppato da HGSI e quindi nella sua piena disponibilità.
Uno solo di questi sviluppi giustificherebbe una quotazione a breve superiore di almeno il 50%.
Altre cose da considerare sono la cassa (se non erro di circa 750 milioni, ma altri possono verificare meglio).
Queste considerazioni mi portano ad avere un TP a sei mesi un anno di circa 31 dollari (non sono bravo a fare queste stime, ma mi sto educando).
La questione che infiamma gli animi, anche quì è l'OPA. next
coxy
coxy
GSK ha già accordi con HGSI. GSK ha la liquidità necessaria per un'OPA?
Altri possono verificare ma credo che le loro immediate disponibilità siano circa 8-9 miliardi di dollari. GSK quota in dollari 36 dollari circa ad azione.
GSK avrebbe dei vantaggi finanziari immediati da una acquisizione? sembra di sì, ma gli esperti potrebbero contribuire su questo punto.
A mio avviso GSK ha molto da guadagnare dall'acquisizione a circa 35-36 dollari (1 a 1 o in cash), tranne in un punto. L'unica incognita negativa è che la forza del progetto HGSI è nella capacità di iniziativa autonoma del capitale umano. L'integrazione in un grande carrozzone potrebbe essere esiziale. Alla GSK si ripropone il quesito dell'uovo o la gallina.
Credo, purtroppo che sceglieranno l'uovo, e lanceranno un'OPA tra non molto. Spero invece che ciò non avvenga. HGSI indipendente genererà più valore e valsente, non solo per gli azionisti.
In conclusione, a mio umile avviso, HGSI nel lungo tempo avrà più valore. nel breve puo' andare incontro ad un'opa. come detto, le mie sono nel cassetto. da seguire nei prossimi due mesi con attenzione.
Altri possono verificare ma credo che le loro immediate disponibilità siano circa 8-9 miliardi di dollari. GSK quota in dollari 36 dollari circa ad azione.
GSK avrebbe dei vantaggi finanziari immediati da una acquisizione? sembra di sì, ma gli esperti potrebbero contribuire su questo punto.
A mio avviso GSK ha molto da guadagnare dall'acquisizione a circa 35-36 dollari (1 a 1 o in cash), tranne in un punto. L'unica incognita negativa è che la forza del progetto HGSI è nella capacità di iniziativa autonoma del capitale umano. L'integrazione in un grande carrozzone potrebbe essere esiziale. Alla GSK si ripropone il quesito dell'uovo o la gallina.
Credo, purtroppo che sceglieranno l'uovo, e lanceranno un'OPA tra non molto. Spero invece che ciò non avvenga. HGSI indipendente genererà più valore e valsente, non solo per gli azionisti.
In conclusione, a mio umile avviso, HGSI nel lungo tempo avrà più valore. nel breve puo' andare incontro ad un'opa. come detto, le mie sono nel cassetto. da seguire nei prossimi due mesi con attenzione.
coxy
coxy
un anno orsono....
GlaxoSmithKline’s darapladib modifies coronary plaque composition and lowers Lp-PLA2 activity, a biomarker predictive of heart attack risk
Results at ESC demonstrated that darapladib:
− Prevented expansion of the necrotic core in human coronary plaques, potentially reducing the risk of plaque rupture and subsequent CV events
− Inhibited activity of plasma Lp-PLA2, an emerging risk factor for CV events
Issued: 11:00 AM, CEST, 10:00 AM BST, 5:00 AM EDT, Tuesday, 2nd Sept 2008
GlaxoSmithKline (GSK) announced today that results of the Integrated Biomarkers and Imaging Study-2 (IBIS-2) showed that use of the selective Lp-PLA2 (lipoprotein-associated phospholipase A2) inhibitor, darapladib, in addition to standard of care treatment, prevented expansion of the necrotic core, a region within coronary plaque associated with a high risk of rupture. Preventing expansion of the necrotic core may reduce the risk of recurrent heart attacks in patients with coronary heart disease (CHD). Although the differences between treatment groups in the primary endpoints of plaque deformability or reduction of the inflammatory biomarker hsCRP were not significant, darapladib significantly reduced activity of the enzyme Lp-PLA2. Numerous studies suggest that high levels of Lp-PLA2 are predictive of coronary heart disease.1
Results of IBIS-2 were presented today at the 2008 Congress of the European Society of Cardiology (ESC) and also were published simultaneously in the American Heart Association’s journal, Circulation.
“Despite many advances in cardiovascular medicine, new approaches are needed to help reduce a patient’s risk of a heart attack, stroke or other cardiovascular event. With darapladib added to current standard therapies, our study suggests that the potential plaque-stabilising effects of darapladib may represent an important approach in treating atherosclerosis and reducing cardiovascular risk,” said Patrick Serruys, MD, PhD, Professor of Medicine, The Erasmus University, Rotterdam, The Netherlands and Chairman of the Steering Committee for IBIS-2.
The year-long Phase II exploratory IBIS-2 trial showed:
− The co-primary endpoints of plaque deformability and plasma levels of hsCRP, showed no significant differences between darapladib and placebo treatment groups, but trended positively.
− Key secondary endpoints showed significant effects of darapladib on plaque composition and plasma levels of Lp-PLA2 activity:
* On average, after 12 months, patients treated with placebo experienced a significant increase in necrotic core volume (p=0.009 vs. baseline) while expansion of the necrotic core was halted in the darapladib-treated group (p=0.71 vs. baseline). This resulted in a significant treatment difference in favour of darapladib (p=0.012 vs. placebo). The effect of darapladib on necrotic core was consistent among several subgroups.
− The activity of circulating Lp-PLA2 was reduced by 59% (p<0.001 vs. placebo).
“The effects of darapladib to reduce expansion of the necrotic core of plaques in the study population provide further confidence that Lp-PLA2 inhibition may prove to be an important therapeutic target,” said Patrick Vallance, MD, Senior Vice President, Drug Discovery, GlaxoSmithKline. “We are committed to the development of darapladib and believe it has the potential to become a major treatment option to help reduce the risk of cardiovascular events.”
About IBIS-2
The IBIS-2 study was a one-year international, randomised, placebo-controlled, parallel-group study in 330 patients with angiographically documented CHD. The study was not powered to address the effects of darapladib on cardiovascular outcomes. IBIS-2 used novel intravascular ultrasound (IVUS) methods, a catheter-based system that allows physicians to acquire images of diseased vessels from inside the artery and to acquire data on plaque composition and deformability. Coronary plaque imaging was obtained in precisely matched segments at baseline and follow-up. Approximately 50% of randomised subjects had evidence of acute coronary syndrome. The study compared the effects of darapladib (once-daily, oral Lp-PLA2 inhibitor, 160 mg/day) to placebo on coronary atheroma deformability (IVUS-palpography) and plasma hsCRP. Secondary endpoints included changes in plaque composition (necrotic core size using VH™ IVUS {virtual histology}), plaque size (IVUS-greyscale), and additional blood biomarkers. During the study, patients received recommended standard of care, including antiplatelet agents (99%) and statins (90%).
Overall, darapladib was well tolerated with no major safety concerns observed. The incidence of adverse events leading to withdrawal was similar with 7% (n=11) in placebo and 4% (n=7) in the darapladib group. There were no differences in the composite of CV death, MI, stroke and coronary revascularisation: Placebo 19%, n=29, darapladib 17% (n=29). Within each organ class, the incidence of adverse events leading to withdrawal was ≤1% in both groups with the exception of 2% (n=4) due to gastrointestinal events in the darapladib group. A higher incidence of malodour (mainly faeces or urine) was reported with darapladib (16%, n=28) compared with placebo (3%, n=5), but was not a common cause of withdrawal from the study (darapladib, 2%, n=3). Routine measurements of systolic blood pressure showed a difference between the groups (darapladib showed mean difference of 3.0 mm Hg, above placebo, p=0.031) that was not previously observed in other clinical trials with darapladib. A post-hoc analysis of intra-arterial blood pressure measured during the IVUS procedure, however, showed no differences in systolic blood pressure between the groups.
About Lp-PLA2
Lp-PLA2 is an enzyme found in blood and atherosclerotic plaque. The underlying process in most heart attacks and strokes is atherosclerosis, which is an inflammatory disease characterised by the build-up of plaque within the walls of arteries. The rupture of unstable atherosclerotic plaque, regardless of the size of the plaque causes most heart attacks and strokes. Enhanced Lp-PLA2 activity has been implicated in the development and progression of atherosclerosis which often leads to heart attacks, strokes and other potentially fatal CV events. Large amounts of Lp-PLA2 are present in the necrotic core of rupture-prone human coronary plaques.
ognuno si renerà facilmente conto che questo "sogno" se divenisse realtà sarebbe il farmaco più venduto sulla Terra.....cosa non semplice, ma è il tipo di farmaco che una gsk cerca...
GlaxoSmithKline’s darapladib modifies coronary plaque composition and lowers Lp-PLA2 activity, a biomarker predictive of heart attack risk
Results at ESC demonstrated that darapladib:
− Prevented expansion of the necrotic core in human coronary plaques, potentially reducing the risk of plaque rupture and subsequent CV events
− Inhibited activity of plasma Lp-PLA2, an emerging risk factor for CV events
Issued: 11:00 AM, CEST, 10:00 AM BST, 5:00 AM EDT, Tuesday, 2nd Sept 2008
GlaxoSmithKline (GSK) announced today that results of the Integrated Biomarkers and Imaging Study-2 (IBIS-2) showed that use of the selective Lp-PLA2 (lipoprotein-associated phospholipase A2) inhibitor, darapladib, in addition to standard of care treatment, prevented expansion of the necrotic core, a region within coronary plaque associated with a high risk of rupture. Preventing expansion of the necrotic core may reduce the risk of recurrent heart attacks in patients with coronary heart disease (CHD). Although the differences between treatment groups in the primary endpoints of plaque deformability or reduction of the inflammatory biomarker hsCRP were not significant, darapladib significantly reduced activity of the enzyme Lp-PLA2. Numerous studies suggest that high levels of Lp-PLA2 are predictive of coronary heart disease.1
Results of IBIS-2 were presented today at the 2008 Congress of the European Society of Cardiology (ESC) and also were published simultaneously in the American Heart Association’s journal, Circulation.
“Despite many advances in cardiovascular medicine, new approaches are needed to help reduce a patient’s risk of a heart attack, stroke or other cardiovascular event. With darapladib added to current standard therapies, our study suggests that the potential plaque-stabilising effects of darapladib may represent an important approach in treating atherosclerosis and reducing cardiovascular risk,” said Patrick Serruys, MD, PhD, Professor of Medicine, The Erasmus University, Rotterdam, The Netherlands and Chairman of the Steering Committee for IBIS-2.
The year-long Phase II exploratory IBIS-2 trial showed:
− The co-primary endpoints of plaque deformability and plasma levels of hsCRP, showed no significant differences between darapladib and placebo treatment groups, but trended positively.
− Key secondary endpoints showed significant effects of darapladib on plaque composition and plasma levels of Lp-PLA2 activity:
* On average, after 12 months, patients treated with placebo experienced a significant increase in necrotic core volume (p=0.009 vs. baseline) while expansion of the necrotic core was halted in the darapladib-treated group (p=0.71 vs. baseline). This resulted in a significant treatment difference in favour of darapladib (p=0.012 vs. placebo). The effect of darapladib on necrotic core was consistent among several subgroups.
− The activity of circulating Lp-PLA2 was reduced by 59% (p<0.001 vs. placebo).
“The effects of darapladib to reduce expansion of the necrotic core of plaques in the study population provide further confidence that Lp-PLA2 inhibition may prove to be an important therapeutic target,” said Patrick Vallance, MD, Senior Vice President, Drug Discovery, GlaxoSmithKline. “We are committed to the development of darapladib and believe it has the potential to become a major treatment option to help reduce the risk of cardiovascular events.”
About IBIS-2
The IBIS-2 study was a one-year international, randomised, placebo-controlled, parallel-group study in 330 patients with angiographically documented CHD. The study was not powered to address the effects of darapladib on cardiovascular outcomes. IBIS-2 used novel intravascular ultrasound (IVUS) methods, a catheter-based system that allows physicians to acquire images of diseased vessels from inside the artery and to acquire data on plaque composition and deformability. Coronary plaque imaging was obtained in precisely matched segments at baseline and follow-up. Approximately 50% of randomised subjects had evidence of acute coronary syndrome. The study compared the effects of darapladib (once-daily, oral Lp-PLA2 inhibitor, 160 mg/day) to placebo on coronary atheroma deformability (IVUS-palpography) and plasma hsCRP. Secondary endpoints included changes in plaque composition (necrotic core size using VH™ IVUS {virtual histology}), plaque size (IVUS-greyscale), and additional blood biomarkers. During the study, patients received recommended standard of care, including antiplatelet agents (99%) and statins (90%).
Overall, darapladib was well tolerated with no major safety concerns observed. The incidence of adverse events leading to withdrawal was similar with 7% (n=11) in placebo and 4% (n=7) in the darapladib group. There were no differences in the composite of CV death, MI, stroke and coronary revascularisation: Placebo 19%, n=29, darapladib 17% (n=29). Within each organ class, the incidence of adverse events leading to withdrawal was ≤1% in both groups with the exception of 2% (n=4) due to gastrointestinal events in the darapladib group. A higher incidence of malodour (mainly faeces or urine) was reported with darapladib (16%, n=28) compared with placebo (3%, n=5), but was not a common cause of withdrawal from the study (darapladib, 2%, n=3). Routine measurements of systolic blood pressure showed a difference between the groups (darapladib showed mean difference of 3.0 mm Hg, above placebo, p=0.031) that was not previously observed in other clinical trials with darapladib. A post-hoc analysis of intra-arterial blood pressure measured during the IVUS procedure, however, showed no differences in systolic blood pressure between the groups.
About Lp-PLA2
Lp-PLA2 is an enzyme found in blood and atherosclerotic plaque. The underlying process in most heart attacks and strokes is atherosclerosis, which is an inflammatory disease characterised by the build-up of plaque within the walls of arteries. The rupture of unstable atherosclerotic plaque, regardless of the size of the plaque causes most heart attacks and strokes. Enhanced Lp-PLA2 activity has been implicated in the development and progression of atherosclerosis which often leads to heart attacks, strokes and other potentially fatal CV events. Large amounts of Lp-PLA2 are present in the necrotic core of rupture-prone human coronary plaques.
ognuno si renerà facilmente conto che questo "sogno" se divenisse realtà sarebbe il farmaco più venduto sulla Terra.....cosa non semplice, ma è il tipo di farmaco che una gsk cerca...
Netzach
Forumer storico
acqua+
ONDA NITRICA
questa Psividia mi piace proprio
però, in una settimana, me ne han date solo 3.200 con 5 ordini di acquisto
missà che per farmi 'na posizione ,,,, cè voion 6 mesi
coxy
coxy
questa Psividia mi piace proprio
però, in una settimana, me ne han date solo 3.200 con 5 ordini di acquisto
missà che per farmi 'na posizione ,,,, cè voion 6 mesi
sei un razzo..... per farmene dare 2400 ho dovuto "spasimare" per un mese
.....non ci sono scambi
come te lo spieghi?
magolibero
..se la sà gira..
http://finance.yahoo.com/news/Novel-EvidenceBased-Systemic-bw-3258858081.html?x=0&.v=1
Novel Evidence-Based Systemic Lupus Erythematosus (SLE) Responder Index Described in Peer Reviewed Publication as Potentially Significant Advance in Lupus Drug Development
Source: Human Genome Sciences, Inc.
On Friday September 4, 2009, 7:00 am EDT
ROCKVILLE, Md.--(BUSINESS WIRE) -- Human Genome Sciences, Inc. (NASDAQ:HGSI - News) today announced publication by the journal Arthritis Care & Research of an article describing the development and use of a novel evidence-based systemic lupus erythematosus (SLE) Responder Index selected as the primary endpoint of two pivotal Phase 3 clinical trials of BENLYSTA™ (belimumab) in serologically active patients with SLE. This primary endpoint was accepted by the FDA under a Special Protocol Assessment agreement for the Phase 3 trials.
“The lack of a gold standard to measure SLE disease activity endorsed by international rheumatology societies or national health authorities has impeded the development of SLE therapies,” said Richard A. Furie, M.D., lead author of the article and Chief, Division of Rheumatology and Allergy-Clinical Immunology, North Shore Long Island Jewish Health System, Lake Success, NY, and Professor of Medicine, Albert Einstein College of Medicine. “In other diseases where manifestations are heterogeneous, combined responder instruments have been used to assess disease activity. We believe the SLE Responder Index may play an important role in drug development for this potentially devastating disease.”
The primary efficacy endpoint of both Phase 3 trials of belimumab is the SLE Responder Index at Week 52, as defined by: (1) a reduction from baseline of at least 4 points on the SELENA SLEDAI disease activity scale (which indicates a clinically important reduction in SLE disease activity); (2) no worsening of disease as measured by the Physician’s Global Assessment (worsening defined as an increase of 0.30 points or more from baseline); and (3) no new BILAG A organ domain score (which indicates a severe flare of lupus disease activity) and no more than one new BILAG B organ domain score (which would indicate a moderate flare of disease activity).
In July 2009, HGS and GSK announced that belimumab met this primary endpoint in BLISS-52, the first of the two Phase 3 trials. Results from BLISS-76, the second Phase 3 trial, are expected in November 2009. Belimumab is being developed by HGS and GSK under a co-development and commercialization agreement entered into in August 2006.
“The SLE Responder Index selected as the primary efficacy endpoint of the BLISS studies of belimumab emerged directly from exploratory analysis of the results of our Phase 2 clinical trial,” said William W. Freimuth, M.D., Ph.D., Vice President, Clinical Research – Immunology, Rheumatology and Infectious Diseases. “This novel and robust index now allows clinical investigators to measure improvement in overall SLE disease activity while at the same time ensuring that the improvement is not accompanied by worsening in other disease manifestations such as organ flares. I am delighted that the validity of the endpoint has now been established with its successful prospective use in the recently completed BLISS-52 study.”
Novel Evidence-Based Systemic Lupus Erythematosus (SLE) Responder Index Described in Peer Reviewed Publication as Potentially Significant Advance in Lupus Drug Development
Source: Human Genome Sciences, Inc.
On Friday September 4, 2009, 7:00 am EDT
ROCKVILLE, Md.--(BUSINESS WIRE) -- Human Genome Sciences, Inc. (NASDAQ:HGSI - News) today announced publication by the journal Arthritis Care & Research of an article describing the development and use of a novel evidence-based systemic lupus erythematosus (SLE) Responder Index selected as the primary endpoint of two pivotal Phase 3 clinical trials of BENLYSTA™ (belimumab) in serologically active patients with SLE. This primary endpoint was accepted by the FDA under a Special Protocol Assessment agreement for the Phase 3 trials.
“The lack of a gold standard to measure SLE disease activity endorsed by international rheumatology societies or national health authorities has impeded the development of SLE therapies,” said Richard A. Furie, M.D., lead author of the article and Chief, Division of Rheumatology and Allergy-Clinical Immunology, North Shore Long Island Jewish Health System, Lake Success, NY, and Professor of Medicine, Albert Einstein College of Medicine. “In other diseases where manifestations are heterogeneous, combined responder instruments have been used to assess disease activity. We believe the SLE Responder Index may play an important role in drug development for this potentially devastating disease.”
The primary efficacy endpoint of both Phase 3 trials of belimumab is the SLE Responder Index at Week 52, as defined by: (1) a reduction from baseline of at least 4 points on the SELENA SLEDAI disease activity scale (which indicates a clinically important reduction in SLE disease activity); (2) no worsening of disease as measured by the Physician’s Global Assessment (worsening defined as an increase of 0.30 points or more from baseline); and (3) no new BILAG A organ domain score (which indicates a severe flare of lupus disease activity) and no more than one new BILAG B organ domain score (which would indicate a moderate flare of disease activity).
In July 2009, HGS and GSK announced that belimumab met this primary endpoint in BLISS-52, the first of the two Phase 3 trials. Results from BLISS-76, the second Phase 3 trial, are expected in November 2009. Belimumab is being developed by HGS and GSK under a co-development and commercialization agreement entered into in August 2006.
“The SLE Responder Index selected as the primary efficacy endpoint of the BLISS studies of belimumab emerged directly from exploratory analysis of the results of our Phase 2 clinical trial,” said William W. Freimuth, M.D., Ph.D., Vice President, Clinical Research – Immunology, Rheumatology and Infectious Diseases. “This novel and robust index now allows clinical investigators to measure improvement in overall SLE disease activity while at the same time ensuring that the improvement is not accompanied by worsening in other disease manifestations such as organ flares. I am delighted that the validity of the endpoint has now been established with its successful prospective use in the recently completed BLISS-52 study.”
magolibero
..se la sà gira..
Webcast
http://finance.yahoo.com/news/Human-Genome-Sciences-Invites-bw-3986588240.html?x=0&.v=1
Human Genome Sciences Invites Investors to Listen to Webcast of Presentation at Thomas Weisel Partners Conference
Source: Human Genome Sciences, Inc.
On Friday September 4, 2009, 8:00 am EDT
ROCKVILLE, Md. --(BUSINESS WIRE)-- Human Genome Sciences, Inc. (NASDAQ:HGSI - News) announced today that its presentation at the 2009 Thomas Weisel Partners Healthcare Conference will be webcast and may be accessed at www.hgsi.com
member of Human Genome Sciences’ senior management team will present a corporate overview on Wednesday, September 9, 2009 at 10:55 am EDT.
Investors interested in listening to the live webcast should log on before the start time in order to download any software required. The archive of the webcast will be available for several days after the live event.
The mission of HGS is to apply great science and great medicine to bring innovative drugs to patients with unmet medical needs. The HGS clinical development pipeline includes novel drugs to treat hepatitis C, lupus, inhalation anthrax and cancer.
HGS and Human Genome Sciences are trademarks of Human Genome Sciences, Inc. For additional information on Human Genome Sciences, Inc., visit the company’s web site at www.hgsi.com
http://finance.yahoo.com/news/Human-Genome-Sciences-Invites-bw-3986588240.html?x=0&.v=1
Human Genome Sciences Invites Investors to Listen to Webcast of Presentation at Thomas Weisel Partners Conference
Source: Human Genome Sciences, Inc.
On Friday September 4, 2009, 8:00 am EDT
ROCKVILLE, Md. --(BUSINESS WIRE)-- Human Genome Sciences, Inc. (NASDAQ:HGSI - News) announced today that its presentation at the 2009 Thomas Weisel Partners Healthcare Conference will be webcast and may be accessed at www.hgsi.com
member of Human Genome Sciences’ senior management team will present a corporate overview on Wednesday, September 9, 2009 at 10:55 am EDT.
Investors interested in listening to the live webcast should log on before the start time in order to download any software required. The archive of the webcast will be available for several days after the live event.
The mission of HGS is to apply great science and great medicine to bring innovative drugs to patients with unmet medical needs. The HGS clinical development pipeline includes novel drugs to treat hepatitis C, lupus, inhalation anthrax and cancer.
HGS and Human Genome Sciences are trademarks of Human Genome Sciences, Inc. For additional information on Human Genome Sciences, Inc., visit the company’s web site at www.hgsi.com