Novartis vende sus Farmacos sin Patente bajo la marca Sandoz.
Sanofi crea una Filial de Fármacos sin Marca para combatir asi la perdida de Patentes , la nueva Filial se llama Pharmacy Healthacare .
Pharma Mar con el tiempo tambien se encontrara con que le iran caducando las Patentes .... pero quien mejor para fabricar Genericos del Yondelis , Aplidin etc etc ... que la propia Pharma Mar o bien creando una nueva Filial de Division de Genericos ....
CAMBIO DE DISCURSO : LA SECOND-LINE SCLC-ES TRAS EL FIASCO DE LA FASE III LAGOON YA MEJOR NI NOMBRARLA...CAMBIAMOS DISCURSO A MANTENIMIENTO EN FIRTS-LINE Y PASAMOS DEL VIAL DE 4 Mg AI VIAL DE 2 Mg .//. JazzPharma TO WITHDRAW LURBINECTEDIN WITH US_FDA IN SECOND-LINE SCLC-ES...EN ESPAÑA NO SE HAN ENTERADO AÚN...SI NO EXISTIERA IMFORTE...AHORA MISMO PHARMAMAR ESTARÍA ANTE UNA GRAVE SITUACIÓN ... 2 DE OCTUBRE DE 2028 ... ES LA FECHA MÁS TEPMPRANA PARA LA POSIBLE ENTRADA DE GENÉRICOS .
21 febrero 2008
20 febrero 2008
19 febrero 2008
18 febrero 2008
Editorial Zeltia publica el Tercer Volumen : El Mundo Submarino - Volumen 3 .

Tras suponer una exitosa venta de los dos primeros volumenes ....sale a la venta el Tercer Volumen .... veremos si en la cuenta de resultados del 2007 nos sorprenden .
Título: El Mundo Submarino de PharmaMar -Volumen 3
ISBN: 978-84-611-8677-8
Edita: Zeltia, S.A. c/ José Abascal, 2 – 28003 Madrid - Teléfono: +34 91 444 4500
Presentación: Tapa dura
Precio: 60,00 € (IVA incluido) Peninsula y Baleares.
Aplidin de Pharma Mar y ARA - C de Pfizer tienen Sinergia en Limfoma y Leucemia , in Vitro e in Vivo .
En Relacion :
Aplidin synergizes with cytosine arabinoside: functional relevance of mitochondria in Aplidin-induced cytotoxicity.Humeniuk R, Menon LG, Mishra PJ, Saydam G, Longo-Sorbello GS, Elisseyeff Y, Lewis LD, Aracil M, Jimeno J, Bertino JR, Banerjee D.
Department of Medicine and Pharmacology, The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA.
Aplidin (plitidepsin) is a novel marine-derived antitumor agent presently undergoing phase II clinical trials in hematological malignancies and solid tumors. Lack of bone marrow toxicity has encouraged further development of this drug for treatment of leukemia and lymphoma. Multiple signaling pathways have been shown to be involved in Aplidin-induced apoptosis and cell cycle arrest in G1 and G2 phase. However, the exact mechanism(s) of Aplidin action remains to be elucidated. Here we demonstrate that mitochondria-associated or -localized processes are the potential cellular targets of Aplidin. Whole genome gene-expression profiling (GEP) revealed that fatty acid metabolism, sterol biosynthesis and energy metabolism, including the tricarboxylic acid cycle and ATP synthesis are affected by Aplidin treatment. Moreover, mutant MOLT-4, human leukemia cells lacking functional mitochondria, were found to be resistant to Aplidin. Cytosine arabinoside (araC), which also generates oxidative stress but does not affect the ATP pool, showed synergism with Aplidin in our leukemia and lymphoma models in vitro and in vivo. These studies provide new insights into the mechanism of action of Aplidin. The efficacy of the combination of Aplidin and araC is currently being evaluated in clinical phase I/II program for the treatment of patients with relapsed leukemia and high-grade lymphoma.
Aplidin synergizes with cytosine arabinoside: functional relevance of mitochondria in Aplidin-induced cytotoxicity.Humeniuk R, Menon LG, Mishra PJ, Saydam G, Longo-Sorbello GS, Elisseyeff Y, Lewis LD, Aracil M, Jimeno J, Bertino JR, Banerjee D.
Department of Medicine and Pharmacology, The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA.
Aplidin (plitidepsin) is a novel marine-derived antitumor agent presently undergoing phase II clinical trials in hematological malignancies and solid tumors. Lack of bone marrow toxicity has encouraged further development of this drug for treatment of leukemia and lymphoma. Multiple signaling pathways have been shown to be involved in Aplidin-induced apoptosis and cell cycle arrest in G1 and G2 phase. However, the exact mechanism(s) of Aplidin action remains to be elucidated. Here we demonstrate that mitochondria-associated or -localized processes are the potential cellular targets of Aplidin. Whole genome gene-expression profiling (GEP) revealed that fatty acid metabolism, sterol biosynthesis and energy metabolism, including the tricarboxylic acid cycle and ATP synthesis are affected by Aplidin treatment. Moreover, mutant MOLT-4, human leukemia cells lacking functional mitochondria, were found to be resistant to Aplidin. Cytosine arabinoside (araC), which also generates oxidative stress but does not affect the ATP pool, showed synergism with Aplidin in our leukemia and lymphoma models in vitro and in vivo. These studies provide new insights into the mechanism of action of Aplidin. The efficacy of the combination of Aplidin and araC is currently being evaluated in clinical phase I/II program for the treatment of patients with relapsed leukemia and high-grade lymphoma.
15 febrero 2008
Iberia podría crear un frente común junto con Clickair, Vueling , Spanair y Air Nostrum .

El Cartel de " Se vende " cuelga de los cielos Españoles .
Publicado hoy en el Expansión .
Escribe Alberto Marimón .
A lo largo de 2008 se van a producir importantes movimientos en la estructura accionarial de las grandes aerolineas Españolas que va a modificar sustancialmente el mapa de los cielos .
El grupo escadinavo SAS cerrara la venta de Spanair ; y Vueling y Clikair empresa participada por Iberia , Air Nostrum ,Quercus- Agroalimen que ya han iniciado contactos para sopesar su Fusion y crear un Gigante Español de los vuelos de bajo coste .
Detras de todas estas operaciones sobresale el nombre propio de Iberia que podría crear un frente comun junto con Clickair, Vueling , Spanair y Air Nostrum .
La unión de Clickair y Vueling tendria como accionista de referencia a Iberia , ademas de Air Nostrum , que posee desde hace años un acuerdo de franquicia con la empresa presidida por Feranado Conte .
A falta de conocer el resultado final , las aerolineas han frenado este ejercicio sus planes comerciales para tratar de poner un poco de orden en el mercado .
Paralelamente a la consolodacion del mercado nacional , queda en el aire la esperada fusión de Iberia con un gran grupo Europeo . Sus directivos llevan años apostando por protagonizar un papel decisivo en el proceso de concentración en Europa , ya sea con British Airways , su socio industrial , o con Air France o a Lufthansa . Sin embargo , lo que toca a hora es poner orden en los cielos nacionales .
14 febrero 2008
NeuroPharma sera la primera en asistir a un Congreso de Relevancia Internacional de Alzheimer .

2008 Feb 12
Preclinical efficacy on GSK-3 inhibitors: Towards a future generation of powerful drugs .
Martinez A.
NeuroPharma, Avda de la Industria 52, 28760 Madrid, Spain.
The renewed interest in glycogen synthase kinase-3 (GSK-3), involved in the molecular pathogenesis of human severe diseases, is focused on the potential of its inhibitors to treat diseases that have significant limitations in their current treatments. During the last 5 years, a lot of literature discuss progress in the search and pharmacological actions of GSK-3 inhibitors, but now, evidence have been accumulated showing preclinical efficacy for these new drugs, in very different models of several distinct pathologies. These studies have been summarized in the present review offering promising examples for new therapies for diabetes, cancer, inflammation, Alzheimer's disease and other neurological pathologies, and mood disorders. Now, clinical human trials are awaiting to confirm the ray of hope that GSK-3 inhibitors are arising for the future treatment of severe unmet diseases. (c) 2008 Wiley Periodicals, Inc. Med Res Rev.
13 febrero 2008
Copyr ... empresa perteneciente al Grupo Zeltia en Italia .

Copyr nasce nel 1961 come Compagnia del Piretro. Da allora il core business dell'azienda è rappresentato dalla formulazione di insetticidi a base di piretro e piretroidi efficaci e con un elevato profilo di sicurezza.
Con l'accresciuta sensibilità alle tematiche ambientali e l'attenzione alla sicurezza di operatori e consumatori, le conoscenze maturate da Copyr nello sviluppo di formulati di derivazione naturale hanno contribuito al consolidamento della propria posizione di leadership sul mercato nazionale e alla continua proposta di nuovi prodotti e settori di applicazione.
A maggio 2006 Copyr viene acquisita da Zelnova S.A., entrando in tal modo a far parte del Gruppo Zeltia.
12 febrero 2008
Aplidin - Melanoma . Articulo en el "" The Journal Pharmacology and experimental Therapeutics "" en su edicion de Marzo .
Plitidepsin has a dual effect inhibiting cell cycle and inducing apoptosis via Rac1/JNK activation in human melanoma cells.
Munoz-Alonso MJ, Gonzalez-Santiago L, Zarich N, Martinez T, Alvarez E, Rojas JM, Munoz A
Instituto de Investigaciones Biomedicas "Alberto Sols" CSIC and Pharma Mar SA.
Melanoma is the most aggressive skin cancer and a serious health problem worldwide because of its increasing incidence and the lack of satisfactory chemotherapy for late stages of the disease. The marine depsipeptide plitidepsin (Aplidin((R))) is an anti-tumoral agent under Phase II clinical development against several neoplasias including melanoma. We report that plitidepsin has a dual effect on the human SK-MEL-28 and UACC-257 melanoma cell lines: at low concentrations (= 45 nM) it inhibits the cell cycle by inducing G1 and G2/M arrest while at higher concentrations it induces apoptosis as assessed by PARP cleavage and the appearance of a hypodiploid peak in flow cytometry analyses. Plitidepsin activates Rac1 GTPase and c-Jun N-terminal kinase (JNK) and, in addition, it induces AKT and p38MAPK phosphorylation. By using inhibitors, we found that JNK and p38MAPK activation depends on Rac1 but not on PI3K, while AKT activation is independent of Rac1 but requires PI3K activity. Plitidepsin cytotoxicity diminishes by Rac1 inhibition or by the blockage of JNK and p38MAPK using SB203580, but not by PI3K inhibition using Wortmannin or LY294002. Remarkably, plitidepsin and dacarbazine, the alkylating agent most active for treating metastatic melanoma, show synergistic anti-proliferative effect that was paralleled at the level of JNK activation. These results indicate that Rac1-JNK activation is critical for cell cycle arrest and apoptosis induction by plitidepsin in melanoma cells. They also support the combined use of plitidepsin and dacarbazine in in vivo studies.
Munoz-Alonso MJ, Gonzalez-Santiago L, Zarich N, Martinez T, Alvarez E, Rojas JM, Munoz A
Instituto de Investigaciones Biomedicas "Alberto Sols" CSIC and Pharma Mar SA.
Melanoma is the most aggressive skin cancer and a serious health problem worldwide because of its increasing incidence and the lack of satisfactory chemotherapy for late stages of the disease. The marine depsipeptide plitidepsin (Aplidin((R))) is an anti-tumoral agent under Phase II clinical development against several neoplasias including melanoma. We report that plitidepsin has a dual effect on the human SK-MEL-28 and UACC-257 melanoma cell lines: at low concentrations (= 45 nM) it inhibits the cell cycle by inducing G1 and G2/M arrest while at higher concentrations it induces apoptosis as assessed by PARP cleavage and the appearance of a hypodiploid peak in flow cytometry analyses. Plitidepsin activates Rac1 GTPase and c-Jun N-terminal kinase (JNK) and, in addition, it induces AKT and p38MAPK phosphorylation. By using inhibitors, we found that JNK and p38MAPK activation depends on Rac1 but not on PI3K, while AKT activation is independent of Rac1 but requires PI3K activity. Plitidepsin cytotoxicity diminishes by Rac1 inhibition or by the blockage of JNK and p38MAPK using SB203580, but not by PI3K inhibition using Wortmannin or LY294002. Remarkably, plitidepsin and dacarbazine, the alkylating agent most active for treating metastatic melanoma, show synergistic anti-proliferative effect that was paralleled at the level of JNK activation. These results indicate that Rac1-JNK activation is critical for cell cycle arrest and apoptosis induction by plitidepsin in melanoma cells. They also support the combined use of plitidepsin and dacarbazine in in vivo studies.
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