Gus
April 1, 1989- October 19, 2009
RIP
My best friend.
Sunday, November 01, 2009
Wednesday, August 19, 2009
Wednesday, July 15, 2009
Who's employed?
ME!
Well now that I'm back in the game in the discovery research business, this site will pick up. I HAVE to! I'm reading now and looking at all things up and coming. This rocks and life is good. Stay tuned. Please come back; this site is will be very informative. No hard feelings towards small biotech but big pharma is good.
Well now that I'm back in the game in the discovery research business, this site will pick up. I HAVE to! I'm reading now and looking at all things up and coming. This rocks and life is good. Stay tuned. Please come back; this site is will be very informative. No hard feelings towards small biotech but big pharma is good.
Tuesday, June 16, 2009
Sorry for the "layoff"
LOL--
I'll try to post the results soon, but I was recently laid off from my job and have been actively pursuing other positions. All is good, a positive attitude will always get you ahead.
Otherwise, there are a handful of companies that are getting good trial data that will be explained here, for one see Jazz Pharma. wow.
Trial information explained tomorrow. Stay positive during hard times!
I'll try to post the results soon, but I was recently laid off from my job and have been actively pursuing other positions. All is good, a positive attitude will always get you ahead.
Otherwise, there are a handful of companies that are getting good trial data that will be explained here, for one see Jazz Pharma. wow.
Trial information explained tomorrow. Stay positive during hard times!
Friday, May 29, 2009
I have several write-ups about some of these abstracts that I'm working on. I'm shutting it down for the rest of today and heading up to Hollywood for the weekend for some R & R.
Check back, when I'm laying by the pool at the London West Hollywood, there may be a post or two. Cheers.
BTW, NVLT is trading now at 74 cents, up a nickel. I see a trend here.....
Check back, when I'm laying by the pool at the London West Hollywood, there may be a post or two. Cheers.
BTW, NVLT is trading now at 74 cents, up a nickel. I see a trend here.....
Wednesday, May 27, 2009
In vivo pharmacokinetic and pharmacodynamic behavior of NOV-002, a redox-modulating glutathione disulfide mimetic
Abstract #4. Session Title: Biochemical Modulators
NOV-002 is a novel formulation of oxidized glutathione (GSSG) currently in a pivotal Phase 3 clinical trial in advanced non-small cell lung cancer. In clinical trials conducted to date, NOV-002 administered in combination with standard chemotherapeutic regimens has resulted in increased efficacy (survival, tumor response) and improved tolerance of standard chemotherapy (e.g. enhanced hematological recovery, immune stimulation). Recently, we showed that the proliferative effects of NOV-002 in the pre-myeloid HL-60 cell line is commensurate with stress-induced S-glutathionylation and activation of kinase pathways (AKT, JAK2 and STAT5) that are known to regulate hematopoiesis. The present investigation was undertaken to characterize the plasma pharmacokinetics of NOV-002 in C57 black mice and to determine if the drug caused S-glutathionylation of plasma proteins that might be used as surrogate biomarkers for drug efficacy. Using HPLC-MS, NOV-002 was measured in plasma at various times following a single intraperitoneal dose. Peak plasma concentrations were observed 10 min following administration of NOV-002 and were diminished by 60 min. Fluorescence based methods were used for quantification of protein thiol content and three S-glutathionylated plasma proteins were identified by mass spectrometry, serine proteinase inhibitor, contrapsin, and a-1-antitrypsin1-6 precursor. These preclinical pharmacokinetic and pharmacodynamic results provide evidence that, as in cell systems, NOV-002 administration in vivo results in generation of a transient oxidative signal that may trigger a variety of redox-regulated biochemical cascades. Such correlates could help to understand and predict clinical responses to treatment with NOV-002.
NOV-002 is a novel formulation of oxidized glutathione (GSSG) currently in a pivotal Phase 3 clinical trial in advanced non-small cell lung cancer. In clinical trials conducted to date, NOV-002 administered in combination with standard chemotherapeutic regimens has resulted in increased efficacy (survival, tumor response) and improved tolerance of standard chemotherapy (e.g. enhanced hematological recovery, immune stimulation). Recently, we showed that the proliferative effects of NOV-002 in the pre-myeloid HL-60 cell line is commensurate with stress-induced S-glutathionylation and activation of kinase pathways (AKT, JAK2 and STAT5) that are known to regulate hematopoiesis. The present investigation was undertaken to characterize the plasma pharmacokinetics of NOV-002 in C57 black mice and to determine if the drug caused S-glutathionylation of plasma proteins that might be used as surrogate biomarkers for drug efficacy. Using HPLC-MS, NOV-002 was measured in plasma at various times following a single intraperitoneal dose. Peak plasma concentrations were observed 10 min following administration of NOV-002 and were diminished by 60 min. Fluorescence based methods were used for quantification of protein thiol content and three S-glutathionylated plasma proteins were identified by mass spectrometry, serine proteinase inhibitor, contrapsin, and a-1-antitrypsin1-6 precursor. These preclinical pharmacokinetic and pharmacodynamic results provide evidence that, as in cell systems, NOV-002 administration in vivo results in generation of a transient oxidative signal that may trigger a variety of redox-regulated biochemical cascades. Such correlates could help to understand and predict clinical responses to treatment with NOV-002.
NOV-002, a redox-modulating glutathione disulfide mimetic, leads to calcium influx and nitric oxide generation through eNOS activation in myeloid c
Abstract 3: Session: NF-kB, Oxidative Stress, and Other Pathways in Cellular Drug Responses
NOV-002, a glutathione disulfide mimetic, is currently in a pivotal Phase 3 clinical trial in advanced non-small cell lung cancer. In clinical trials conducted to date, NOV-002 administered in combination with standard chemotherapeutic regimens has resulted in increased efficacy (survival, tumor response) and improved tolerance of standard chemotherapy (e.g. enhanced hematological recovery, immune stimulation). Recently, we showed that the myeloproliferative effect of NOV-002 in the pre-myeloid HL-60 cell line occurs in parallel with stress-induced S-glutathionylation and activation of kinase pathways (AKT, JAK2 and STAT5) that are known to regulate hematopoiesis. NOV-002 treatment produces oxidant signals intracellularly and at the cell surface. HL60 cells express the cell surface enzyme gamma-glutamyl transpeptidase (GGT). NOV-002 is a substrate for GGT and its cleavage alters the intracellular redox potential. Here we show that NOV-002 treatment in HL60 cells mediates changes of the plasma membrane electrical potential as detected by the fluorescent probe, bisOxonal. These changes were concurrent with time- and dose-dependent increases in the accumulation of intracellular Ca2+ as detected by Fura-2-AM and Fluo-3-AM fluorescent dyes. These effects were abolished by the addition of an extracellular Ca2+ chelator (EGTA) and decreased by the intracellular chelator, BAPTA-AM. These data suggest that NOV-002 induced calcium signaling involves entry of extracellular Ca2+ across the plasma membrane. Microarray analyses highlighted that NOV-002 treatment impacts expression of proteins involved in calcium signaling and nitric oxide (NO) metabolism pathways. NO generation following NOV-002 treatment was decreased by ~80% in HL60 cells transfected with siRNA to deplete eNOS levels. Overall, NOV-002 mediated alteration of cell surface redox status and transmembrane potential resulted in an induction of calcium influx, followed by NO generation through eNOS activation. These events may be pertinent to myeloproliferation that has been observed in cancer patients treated with NOV-002 plus standard chemotherapy.
NOV-002, a glutathione disulfide mimetic, is currently in a pivotal Phase 3 clinical trial in advanced non-small cell lung cancer. In clinical trials conducted to date, NOV-002 administered in combination with standard chemotherapeutic regimens has resulted in increased efficacy (survival, tumor response) and improved tolerance of standard chemotherapy (e.g. enhanced hematological recovery, immune stimulation). Recently, we showed that the myeloproliferative effect of NOV-002 in the pre-myeloid HL-60 cell line occurs in parallel with stress-induced S-glutathionylation and activation of kinase pathways (AKT, JAK2 and STAT5) that are known to regulate hematopoiesis. NOV-002 treatment produces oxidant signals intracellularly and at the cell surface. HL60 cells express the cell surface enzyme gamma-glutamyl transpeptidase (GGT). NOV-002 is a substrate for GGT and its cleavage alters the intracellular redox potential. Here we show that NOV-002 treatment in HL60 cells mediates changes of the plasma membrane electrical potential as detected by the fluorescent probe, bisOxonal. These changes were concurrent with time- and dose-dependent increases in the accumulation of intracellular Ca2+ as detected by Fura-2-AM and Fluo-3-AM fluorescent dyes. These effects were abolished by the addition of an extracellular Ca2+ chelator (EGTA) and decreased by the intracellular chelator, BAPTA-AM. These data suggest that NOV-002 induced calcium signaling involves entry of extracellular Ca2+ across the plasma membrane. Microarray analyses highlighted that NOV-002 treatment impacts expression of proteins involved in calcium signaling and nitric oxide (NO) metabolism pathways. NO generation following NOV-002 treatment was decreased by ~80% in HL60 cells transfected with siRNA to deplete eNOS levels. Overall, NOV-002 mediated alteration of cell surface redox status and transmembrane potential resulted in an induction of calcium influx, followed by NO generation through eNOS activation. These events may be pertinent to myeloproliferation that has been observed in cancer patients treated with NOV-002 plus standard chemotherapy.
The role of polymorphisms of glutathione S-transferase pi in redox regulation through protein S-glutathionylation
Abstract #2: Session: Resistance to Antitubulin Drugs, Resistance to Platinums, and Glutathione Metabolism
Glutathione S-transferase P1-1 (GSTP) is a prominent and ubiquitously expressed enzyme protein in many human cancers. Its expression is increased in response to a variety of apparently unrelated stress conditions and high levels (sometimes ~1-2% of cytosolic protein) are frequently linked to drug resistance phenotypes, even when the selecting drug is not a substrate for the enzyme. While recent results have shown that GSTP interacts non-covalently with kinases, it has always seemed probable that a more prevalent cellular function may be ascribed to such a common protein. Recently, we have demonstrated by in vitro and in vivo approaches that the catalytic properties of GSTP are critical to the post-translational S-glutathionylation of cysteine residues in a number of different target proteins (Townsend et al, JBC 2009). Genetic polymorphisms of GSTP have differing catalytic constants for some small molecule substrates. In the present studies, we evaluated the role of GSTP polymorphisms in regulating S-glutathionylation reactions. We generated stably transfected HEK293 cells expressing the four human GSTP*A-D alleles (Ile105/Ala114; Val105/Ala114; Val105/Val114; and Ile105/Val114) and a catalytically inactive mutant. In response to two drugs, NOV-002, a glutathione disulfide mimetic and PABA/NO, a nitric oxide releasing prodrug, cells mount a rapid S-glutathionylation of specific target proteins. The rate of protein S-glutathionylation is significantly enhanced by the presence of a catalytically active (intact tyr7 residue) GSTP and is also is greater for the GSTP*A and *D alleles. A role for GSTP in the catalytic formation of a disulfide between the thiolate of GSH and a low pK cysteine thiol in a target protein is a novel property for GSTP. The differential susceptibility to cancer initiation and drug response associated with some GSTP polymorphisms may be attributable to the their capacity to respond to oxidative and nitrosative stress through protein S-glutathionylation.
Inhibition of tumor cell invasion and ErbB2/PI3K signaling pathways by the glutathione disulfide-mimetic NOV-002
Abstract #1:
NOV-002, a glutathione disulfide-mimetic, is in advanced clinical development for oncology indications. It is believed to act by modulating intracellular and cell surface redox status resulting in a pleiotropic pharmacologic profile. Here we report the ability of NOV-002 to inhibit the invasiveness of human tumor cells in vitro by suppressing the activation of a well-characterized, redox sensitive signaling pathway that is critical for tumor cell growth and invasion. In the Matrigel invasion assay, NOV-002 inhibited the invasion of a variety of human tumor cell lines including A549 (non-small cell lung), MDA-MB436 (breast), SKOV3 (ovarian) and HCT-15, HCT-116 and Colo205 (colorectal) in a dose-dependent manner with IC50s between 17.7mM and 91mM. In contrast, cell migration was only inhibited in the colorectal tumor cell lines suggesting that NOV-002 may affect pathways which are specific for invasion. 1 mM NOV-002 (the highest concentration tested in the invasion and migration assays) was not toxic to any of the tumor cell lines studied even after 72 hours of culture using MTT viability assay. These effects were shown to involve the suppression of ErbB2 and phosphoinositide-3 kinase (PI3K) pathways by NOV-002. Immunoblot analysis demonstrated that NOV-002 reduced the expression of the phosphorylated (active) forms of signaling proteins ErbB2 and PI3k, known to regulate tumor cell invasion in A549 and Colo205 cells, without affecting the total amount of these proteins. Activation of Akt and RhoA, downstream molecules of the ErbB2/PI3K pathway, was also inhibited by NOV-002. Thus in both A549 and Colo205 cell lines, the active form of both upstream (ErbB2 and PI3K) and downstream (Akt and RhoA) signaling proteins were suppressed by NOV-002 at concentrations between 30 mM and 1 mM in a dose-dependent manner. Inhibition was more pronounced at 24 hours post-exposure compared to 8 or 16 hours. In prostate cancer PC3 cells which are not affected by NOV-002 in the invasion assay, suppression of ErbB2/PI3K signaling pathway was not observed. Thus, inhibition of tumor cell invasion by NOV-002 may be due to the inhibition of the ErbB2/PI3K signaling pathway activation that controls this process. We have previous shown that ERp5, a member of the redox-regulated protein disulfide isomerase family, promotes tumor cell invasion by activating the ErbB2/PI3K pathway. Thus ERp5 may represent a direct target for NOV-002. These results also indicate that NOV-002 may have particular therapeutic benefit in the treatment of cancers that utilize ErbB2 and PI3K pathway activation.
I'll get them all posted and then try to explain some science.
NOV-002, a glutathione disulfide-mimetic, is in advanced clinical development for oncology indications. It is believed to act by modulating intracellular and cell surface redox status resulting in a pleiotropic pharmacologic profile. Here we report the ability of NOV-002 to inhibit the invasiveness of human tumor cells in vitro by suppressing the activation of a well-characterized, redox sensitive signaling pathway that is critical for tumor cell growth and invasion. In the Matrigel invasion assay, NOV-002 inhibited the invasion of a variety of human tumor cell lines including A549 (non-small cell lung), MDA-MB436 (breast), SKOV3 (ovarian) and HCT-15, HCT-116 and Colo205 (colorectal) in a dose-dependent manner with IC50s between 17.7mM and 91mM. In contrast, cell migration was only inhibited in the colorectal tumor cell lines suggesting that NOV-002 may affect pathways which are specific for invasion. 1 mM NOV-002 (the highest concentration tested in the invasion and migration assays) was not toxic to any of the tumor cell lines studied even after 72 hours of culture using MTT viability assay. These effects were shown to involve the suppression of ErbB2 and phosphoinositide-3 kinase (PI3K) pathways by NOV-002. Immunoblot analysis demonstrated that NOV-002 reduced the expression of the phosphorylated (active) forms of signaling proteins ErbB2 and PI3k, known to regulate tumor cell invasion in A549 and Colo205 cells, without affecting the total amount of these proteins. Activation of Akt and RhoA, downstream molecules of the ErbB2/PI3K pathway, was also inhibited by NOV-002. Thus in both A549 and Colo205 cell lines, the active form of both upstream (ErbB2 and PI3K) and downstream (Akt and RhoA) signaling proteins were suppressed by NOV-002 at concentrations between 30 mM and 1 mM in a dose-dependent manner. Inhibition was more pronounced at 24 hours post-exposure compared to 8 or 16 hours. In prostate cancer PC3 cells which are not affected by NOV-002 in the invasion assay, suppression of ErbB2/PI3K signaling pathway was not observed. Thus, inhibition of tumor cell invasion by NOV-002 may be due to the inhibition of the ErbB2/PI3K signaling pathway activation that controls this process. We have previous shown that ERp5, a member of the redox-regulated protein disulfide isomerase family, promotes tumor cell invasion by activating the ErbB2/PI3K pathway. Thus ERp5 may represent a direct target for NOV-002. These results also indicate that NOV-002 may have particular therapeutic benefit in the treatment of cancers that utilize ErbB2 and PI3K pathway activation.
I'll get them all posted and then try to explain some science.
NVLT.OB at AACR 2009
I have the abstracts they presented, sans the figures. I will post them shortly as they download.
NVLT is trading at 64 cents today.
NVLT is trading at 64 cents today.
Monday, May 25, 2009
Tuesday, April 14, 2009
Dendreon blows up on Cancer Vaccine Data
NEW YORK, April 14 (Reuters) - An experimental medicine from Dendreon Corp improved survival in men with advanced forms of prostate cancer, the company said on Tuesday, bolstering chances of it becoming the first approved therapeutic vaccine for any type of cancer.
Shares of Dendreon (DNDN.O) more than tripled in heavy morning trading to as high as $22.10 and were up 138 percent at $17.38 in afternoon trade as the study results suggested a revolutionary form of therapy is on the horizon for one of the most common cancers.
Unlike traditional vaccines that prevent disease, the company's Provenge medicine treats it by stimulating the body's own immune system.
"If you're in late stages of prostate cancer and your doctor says, 'You'll have no side effects with this drug and it will probably extend your life,' who's not going to take it?" said Sven Borho, an analyst with OrbiMed Advisors.
The Phase III clinical trial met the main study goal of improving survival, prompting Dendreon to say it will seek U.S. regulatory approval of Provenge in the fourth quarter.
"The successful outcome from the Phase 3 IMPACT study provides validation of the long-pursued goal of harnessing the human immune system against a patient's own cancer," Dendreon Chief Executive Mitchell Gold said in a statement.
Prostate cancer is the most common cancer in American men other than skin cancers, according to the American Cancer Society. About one in six men will be diagnosed with prostate cancer during his lifetime.
Paul Latta, an analyst with McAdams Wright Ragen, said Provenge stood to be a $200 million product if it is approved only in the advanced prostate cancer patient group, but could expand to a $1 billion blockbuster if it is expanded to men with earlier stages of the disease.
But Borho, whose New York investment firm owns 2.5 million shares of Dendreon, said Provenge's annual sales could reach several billion dollars.
"Dendreon has delivered the goods for sure, this is very exciting," Borho said.
More in depth drug overview this afternoon. I will attempt to show you how it works. Stay tuned.
Tuesday, February 24, 2009
MAP Pharmaceutical shares fall after asthma drug candidate fails late-stage study
MAP Pharmaceuticals, Inc., a development stage company, focuses on developing drug candidates to treat local respiratory and treatable diseases. It develops inhalable drug particles to facilitate pulmonary delivery.
The company's proprietary product candidates in clinical development include Unit Dose Budesonide, a nebulized version of budesonide for the treatment of pediatric asthma in children; and MAP0004, an orally inhaled version of dihydroergotamine for the treatment of migraine. Its product portfolio also includes the earlier stage product candidates, which include MAP0005, an inhaled corticosteroid and beta-agonist for the treatment of asthma and chronic obstructive pulmonary disease; and MAP0001, a formulation of insulin for the treatment of Type 1 and Type 2 diabetes through pulmonary delivery using Tempo inhaler.
The company has a research and development, license, and supply agreement with Eiffel Technologies Limited to develop certain methods for manufacturing formulations of beta-agonists, alone or with steroid, steroids, or insulin; and a license agreement with Nektar Therapeutics UK Limited to develop and commercialize various formulations of a form of dihydroergotamine for administration by inhalation using a device.
NEW YORK -- Shares of MAP Pharmaceuticals Inc. fell in premarket trading, after the drug developer said its experimental treatment for children with asthma failed to meet its main goal in a late-stage study.
The stock fell as low as $4.20 in premarket trading, after closing at $11.03 during the regular session Monday. Shares have traded between $1.75 and $14.97 over the last 52 weeks.
Late Monday, the Mountain View, Calif.-based company said a Phase III trial studying two doses of Unit Dose Budesonide showed the drug, which is a fine mist version of the steroid budesonide, didn't control asthma better than placebo. The study assessed changes from baseline in nighttime and daytime symptom scores, including cough, wheeze and shortness of breath.
The study included 360 children ages 12 months to eight years who had never taken steroids, and who received either 0.25 of a milligram of the drug, 0.135mg, or a placebo twice a day for 12 weeks.
MAP's partner on the drug candidate is AstraZeneca PLC.
Deutsche Bank-North America analyst David M. Steinberg downgraded shares of MAP to "Hold" from "Buy" and cut the price target to $5 from $15.
"Out of MAP's two Phase 3 pipeline products, the UDB program had been the one that offered lower risk along with higher potential peak sales," he said, in a note to investors.
Though another late-stage program, focusing on chronic migraines, could still generate more than $250 million in annual revenue, he added, the company's current value is not justified and the development risks have increased.
"This negative result is quite surprising given the overall positive results for the previously conducted Phase 2 trial, AstraZeneca's recently signed lucrative partnership for this compound, and the long track record of the base molecule budesonide," he said.
The stock ended trading today valued at $2.65. Cash value?
an explanation of the drug and how it works coming in the am.
The company's proprietary product candidates in clinical development include Unit Dose Budesonide, a nebulized version of budesonide for the treatment of pediatric asthma in children; and MAP0004, an orally inhaled version of dihydroergotamine for the treatment of migraine. Its product portfolio also includes the earlier stage product candidates, which include MAP0005, an inhaled corticosteroid and beta-agonist for the treatment of asthma and chronic obstructive pulmonary disease; and MAP0001, a formulation of insulin for the treatment of Type 1 and Type 2 diabetes through pulmonary delivery using Tempo inhaler.
The company has a research and development, license, and supply agreement with Eiffel Technologies Limited to develop certain methods for manufacturing formulations of beta-agonists, alone or with steroid, steroids, or insulin; and a license agreement with Nektar Therapeutics UK Limited to develop and commercialize various formulations of a form of dihydroergotamine for administration by inhalation using a device.
NEW YORK -- Shares of MAP Pharmaceuticals Inc. fell in premarket trading, after the drug developer said its experimental treatment for children with asthma failed to meet its main goal in a late-stage study.
The stock fell as low as $4.20 in premarket trading, after closing at $11.03 during the regular session Monday. Shares have traded between $1.75 and $14.97 over the last 52 weeks.
Late Monday, the Mountain View, Calif.-based company said a Phase III trial studying two doses of Unit Dose Budesonide showed the drug, which is a fine mist version of the steroid budesonide, didn't control asthma better than placebo. The study assessed changes from baseline in nighttime and daytime symptom scores, including cough, wheeze and shortness of breath.
The study included 360 children ages 12 months to eight years who had never taken steroids, and who received either 0.25 of a milligram of the drug, 0.135mg, or a placebo twice a day for 12 weeks.
MAP's partner on the drug candidate is AstraZeneca PLC.
Deutsche Bank-North America analyst David M. Steinberg downgraded shares of MAP to "Hold" from "Buy" and cut the price target to $5 from $15.
"Out of MAP's two Phase 3 pipeline products, the UDB program had been the one that offered lower risk along with higher potential peak sales," he said, in a note to investors.
Though another late-stage program, focusing on chronic migraines, could still generate more than $250 million in annual revenue, he added, the company's current value is not justified and the development risks have increased.
"This negative result is quite surprising given the overall positive results for the previously conducted Phase 2 trial, AstraZeneca's recently signed lucrative partnership for this compound, and the long track record of the base molecule budesonide," he said.
The stock ended trading today valued at $2.65. Cash value?
an explanation of the drug and how it works coming in the am.
For Lack of better data.....YIKES
La Jolla Pharma:
SAN DIEGO--La Jolla Pharmaceutical Company (Nasdaq: LJPC - News) today announced that, following the negative results of the Riquent Phase 3 interim efficacy analysis, the Company is taking steps to reduce costs to preserve its remaining cash and other assets, including a substantial reduction in personnel and other operating expenses. In addition to working to maximize the value of the Company’s cash and remaining assets, the Company is evaluating strategic options such as winding down the business or the sale of the Company.
"We are very disappointed that the Riquent® program was not successful,” said Deirdre Y. Gillespie, M.D., President and CEO of La Jolla Pharmaceutical Company. “Following the receipt of the interim efficacy results, we have undertaken activities to rapidly reduce costs, paring down to the minimum necessary to carry out basic operations and address contractual obligations. Unfortunately, Riquent was our sole significant asset. The only other program in our research pipeline targeted SSAO inhibitors which are at an early preclinical stage and of minimum value.”
ummmm....DONE. Sorry to hear this.
This gloom is still not getting me down, I think Bio Tech is in rebound and more clinical data and interpretation is on the way! Stay positive.
SAN DIEGO--La Jolla Pharmaceutical Company (Nasdaq: LJPC - News) today announced that, following the negative results of the Riquent Phase 3 interim efficacy analysis, the Company is taking steps to reduce costs to preserve its remaining cash and other assets, including a substantial reduction in personnel and other operating expenses. In addition to working to maximize the value of the Company’s cash and remaining assets, the Company is evaluating strategic options such as winding down the business or the sale of the Company.
"We are very disappointed that the Riquent® program was not successful,” said Deirdre Y. Gillespie, M.D., President and CEO of La Jolla Pharmaceutical Company. “Following the receipt of the interim efficacy results, we have undertaken activities to rapidly reduce costs, paring down to the minimum necessary to carry out basic operations and address contractual obligations. Unfortunately, Riquent was our sole significant asset. The only other program in our research pipeline targeted SSAO inhibitors which are at an early preclinical stage and of minimum value.”
ummmm....DONE. Sorry to hear this.
This gloom is still not getting me down, I think Bio Tech is in rebound and more clinical data and interpretation is on the way! Stay positive.
Friday, February 20, 2009
New Posting Rule:
I am back to posting and will post new events everyday. This site still gets too many hits to avoid and i'm really enthused that biotech is making a comeback in the current market.
I am more and more encouraged everyday. Also check out www.whatisthatdrug.com ; there are a ton of new drugs for everything that you all should know about.
I am very happy about: ANDS
YTD: over 300% upswing! F-off HCV.
I am more and more encouraged everyday. Also check out www.whatisthatdrug.com ; there are a ton of new drugs for everything that you all should know about.
I am very happy about: ANDS
YTD: over 300% upswing! F-off HCV.
Friday, January 09, 2009
Take that HCV!!!
Anadys goes through the roof on ANA598 data:
Anadys Pharmaceuticals released the first antiviral activity data on its lead hepatitis C drug Thursday, which the company hopes will attract a deep-pocketed partner to fund further development.
Eight patients with hepatitis C treated with a twice-daily dose of the drug ANA598 reported a median reduction of more than 99% in the level of virus after three days of treatment, the company said.
None of the patients in the study reported a rebound in their viral loads while taking the drug and there were no serious adverse events reported. The interim results come from an ongoing phase Ib study of ANA598 -- the first study in which the drug is being tested in patients infected with hepatitis C.
Anadys CEO Steven Worland heralded the early data on ANA598, calling the magnitude of the viral load drop shown by ANA598 greater than what's been reported by any other competing drug in its class.
ANA598 is what is known as a non-nucleoside polymerase inhibitor. These drugs act directly against specific enzymes to prevent the hepatitis C virus from making copies of itself. That's different from current treatments for hepatitis C, namely long-acting forms of interferon and a drug called ribavirin, which work by stimulating the body's immune system to destroy the virus.
Pfizer, Gilead Sciences and Merk also are working on non-nucleoside polymerase inhibitors for hepatitis C.
Anadys shares fell below $2 at the end of 2008 in part because the company, with about $25 million to $27 million in the bank, needs to raise money. Worland says the company's goal is to use the new data on ANA598 to attract a corporate partner that will pour money into the company and help future studies of the drug.
Hey Pam Anderson, are you interested? HCV is very interesting organism. If you want more info just leave me a comment, thanks.
article cited via thestreet.com
Anadys Pharmaceuticals released the first antiviral activity data on its lead hepatitis C drug Thursday, which the company hopes will attract a deep-pocketed partner to fund further development.
Eight patients with hepatitis C treated with a twice-daily dose of the drug ANA598 reported a median reduction of more than 99% in the level of virus after three days of treatment, the company said.
None of the patients in the study reported a rebound in their viral loads while taking the drug and there were no serious adverse events reported. The interim results come from an ongoing phase Ib study of ANA598 -- the first study in which the drug is being tested in patients infected with hepatitis C.
Anadys CEO Steven Worland heralded the early data on ANA598, calling the magnitude of the viral load drop shown by ANA598 greater than what's been reported by any other competing drug in its class.
ANA598 is what is known as a non-nucleoside polymerase inhibitor. These drugs act directly against specific enzymes to prevent the hepatitis C virus from making copies of itself. That's different from current treatments for hepatitis C, namely long-acting forms of interferon and a drug called ribavirin, which work by stimulating the body's immune system to destroy the virus.
Pfizer, Gilead Sciences and Merk also are working on non-nucleoside polymerase inhibitors for hepatitis C.
Anadys shares fell below $2 at the end of 2008 in part because the company, with about $25 million to $27 million in the bank, needs to raise money. Worland says the company's goal is to use the new data on ANA598 to attract a corporate partner that will pour money into the company and help future studies of the drug.
Hey Pam Anderson, are you interested? HCV is very interesting organism. If you want more info just leave me a comment, thanks.
article cited via thestreet.com
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