The FDA approval for Provenge was based on clinical data that showed a 4 month increase in survival showing a 25.8 month survival with Provenge compared to 21.6 months for the placebo injection. However the placebo injection has come under scrutiny and probably reduces survival which shows a false life extension.
This anomoly is highlighted by results from the latest Zytiga trial which showed that patients who were treated with the placebo lived for 27.2 months which is actually longer than people treated with Provenge. So a true placebo shows a survival of 27.2 months, Provenge shows a survival of 25.8 months, and the Provenge Placebo group had a survival of 21.6 months. These figures clearly show that the Provenge Placebo is toxic and actually causes decreased survival. In view of this decreased survival using a Provenge Placebo vaccine raises issues about the ethics of giving such a treatment to terminally ill men with prostate cancer.
Sunday, 25 November 2012
Does Provenge Work for Men with Prostate Cancer ?
Does Provenge Work for Men with Prostate Cancer - Well the short answer is No ! There is as yet no clinical evidence for the Provenge vaccine working in practise and men treated with Provenge continue to experience rises in PSA and disease progression.
This same question was asked on a website www.prostate.net
that is promoting Provenge and other bogus treatments such as "Prost-P10X" and prostate cancer sufferers should be wary of the products peddled on this website and the information it contains which encourages allopathic approaches such as surgery radiotherapy and provenge.
So far the only testimonials relating to Provenge use appear to be negative and here is one example.
Provenge Testimonial
This same question was asked on a website www.prostate.net
that is promoting Provenge and other bogus treatments such as "Prost-P10X" and prostate cancer sufferers should be wary of the products peddled on this website and the information it contains which encourages allopathic approaches such as surgery radiotherapy and provenge.
So far the only testimonials relating to Provenge use appear to be negative and here is one example.
Provenge Testimonial
"I spent the day having CT and Bone scans, then talking with ONC about the results. Apparently Provenge did absolutely nothing. I have a couple of new mets and PSA has gone from 14 at time of Provenge treatment to 49 two months later. What a bummer.
That is $93,000, a bunch of time and a couple of crappy days down the drain for nothing.
Has anybody heard of Provenge doing nothing? I knew it was not a cure, but I thought it would buy me six months to a year before having to do something else.
ONC says I either need to start on Taxotere or get into a trial. I do not want to do Taxotere, but she says if I do one treatment and claim I can not tolerate it I can then start Zytiga. That is probably what I will do.
Has not been a good day.
Some days you are the pigeon and some days you are the statue. Today I know which one I am.
That is $93,000, a bunch of time and a couple of crappy days down the drain for nothing.
Has anybody heard of Provenge doing nothing? I knew it was not a cure, but I thought it would buy me six months to a year before having to do something else.
ONC says I either need to start on Taxotere or get into a trial. I do not want to do Taxotere, but she says if I do one treatment and claim I can not tolerate it I can then start Zytiga. That is probably what I will do.
Has not been a good day.
Some days you are the pigeon and some days you are the statue. Today I know which one I am.
I know Provenge does not necessarily effect one's PSA. However, you should not get new metastases after you had it, and any bone mets you already have should not get any worse. In just two months since I was treated the metastasis I already had got worse and new ones appeared. That is a sure sign that Provenge did not work. I have spoken with two Oncs about this and they agree that this should not be happening. Regardless of what your PSA does you will not live long if you continue to get new and bigger mets. You can not sit around hoping maybe it will start working in a month or two.
Needless to say I am very disappointed that Provenge did not perform as advertised in my case. I was counting on it to give me a year or so before I had to move on to another treatment. By then I was hoping that MDV3100 would be approved and who knows what else may come along.
Knowing what I knew in March I would do it again. However, at this point it was as I said a waste of time, money, and a lot of people's efforts. All the research I did beforehand never mentioned that some people got zero benefit from it.
However, the Onc I saw today, who is the biggest Provenge guy here in the USA
Norm
Saturday, 17 November 2012
EMA Committee Recommends Zytiga Before Chemotherapy
The European Medicines Agency (EMA) advisory body the CHMP have recommended Zytiga for use before chemotherapy in treating prostate cancer. This paves the way for final EMA approval which is expected soon. Zytiga is also undergoing consideration by the FDA for use before chemotherapy. This will help thousands of men who have been looking forward to this approval.
CHMP backed expanding the label of Zytiga (abiraterone acetate) to include treatment in combination with prednisone or prednisolone of chemotherapy-naïve patients with metastatic castration-resistant prostate cancer (CRPC) who are asymptomatic or mildly asymptomatic after failing androgen deprivation therapy. Zytiga is under Priority Review by the FDA for this indication in the US, with a decision date expected in December. Zytiga is already approved in the US and EU in combination with prednisone to treat metastatic CRPC patients who have received prior chemotherapy containing docetaxel.
CHMP backed expanding the label of Zytiga (abiraterone acetate) to include treatment in combination with prednisone or prednisolone of chemotherapy-naïve patients with metastatic castration-resistant prostate cancer (CRPC) who are asymptomatic or mildly asymptomatic after failing androgen deprivation therapy. Zytiga is under Priority Review by the FDA for this indication in the US, with a decision date expected in December. Zytiga is already approved in the US and EU in combination with prednisone to treat metastatic CRPC patients who have received prior chemotherapy containing docetaxel.
Friday, 16 November 2012
Zytiga Approved in Ireland
Zytiga has at long last been approved for use in Ireland as from the 1st of December 2012. Initially this treatment, also known as Abiraterone was rejected by the Irish regulatory board NCPE (National Centre for Pharmaco Economics) on cost grounds. However after negotiations with the manufacturer Johnson & Johnson a reduced price has been agreed meaning that this treatment will now be available in Ireland. From 1st of December Zytiga will be available on the national health system for use to treat advanced prostate cancer in men who have relapsed following chemotherapy.
Professor Gerry Potter the inventor of Zytiga has recently been on a lecture tour of Ireland visiting Dublin, Cork and Galway finally giving a public talk to the Ballinasloe Cancer Support Group on the discovery of Zytiga and Salvestrols. After the talk Prof Potter said "I am delighted that men in Ireland can now benefit from Zytiga and all the research that we have done. Hopefully Zytiga will be approved soon for use as an earlier treatment before chemotherapy is even needed".
Medical professionals have hailed the news that Zytiga will soon be available inIreland as really good news
It is the second most frequent male cancer and claims the lives of 500 men a year in Ireland alone.
There are almost 17,000 suffering with the disease at the moment andIreland Europe . Consultant oncologist at Tallaght and St Vincent 's Hospital Dr Ray McDermott said it is huge progress for prostate cancer sufferers here.
He added: "This is great news for Irish patients and their families.
"Up to now there has been no active treatment available for patients with advanced prostate cancer whose cancer has progressed after chemotherapy so this new treatment represents a real un-met clinical need." The drug will be reimbursed by health authorities here from December 1. John Dowling from the Men Against Cancer said it will give patients precious months more to live.
He added: "Men with advanced prostate cancer, if suitable, may now be offered treatment with abiraterone which may give them the real prospect of precious additional months over current treatments together with a reasonable quality of life."
.
In Ireland Ireland
Zytiga (abiraterone acetate) was approved originally for patients who had relapsed after multiple forms of ther-apy, including chemotherapy. Approvals following the initial COU-AA-301 Phase III study (the ‘301 Study’) were based on results from an interim analysis showing a statistically significant improvement in overall survival and an acceptable safety profile. Zytiga, in combination with prednisone, was approved by the European Medicines Agency (EMA) in September 2011 for the treatment of metastatic, castration-resistant prostate cancer (mCRPC) in adult men whose disease has progressed on or after a docetaxel-based chemotherapy regimen.
“As of this moment, abiraterone acetate is not available to patients inIreland
The drug is currently licensed for more advanced patients, who have already received chemotherapy. Its manufacturer, Janssen, is currently in talks with the National Cancer Control Programme on reimbursement for patients, similar to those in the 301 Study.
Shows great promise
Dr McDermott said: “This is an oral agent which shows great promise for patients with advanced prostate cancer, is well tolerated and improves quality of life.”
In addition, an application to the EMA’s Committee for Medicinal Products for Human Use (CHMP) is intended to extend the use of abiraterone acetate administered with prednisone for the treatment of patients with mCRPC who are asymptomatic or mildly symptomatic, after failure of androgen deprivation therapy and before chemotherapy.
Submissions have been made, based on Phase III results, which show “significant improvement” in radiographic progression-free survival and a trend for increased overall survival in patients receiving Zytiga plus prednisone.
The COU-AA-302 trial (the ‘302 Study’) was for patients who had progressed on androgen deprivation therapies but had not yet received chemotherapy.
This study, which included 1,088 asymptomatic or mildly symptomatic men with mCRPC who had not received chemotherapy, evaluated the effect of abiraterone acetate plus prednisone on the co-primary endpoints of radiographic progression-free survival (rPFS) and overall survival (OS) compared to placebo plus prednisone. Data from this study were presented at the 48th Annual Meeting of the American Society of Clinical Oncology (ASCO).
The study was designed with patients in mind who had progressed after standard androgen deprivation therapy. In most parts of the world, this involves either medical (with LHRH agonists) or surgical castration.
Often, an anti-androgen such as bicalutamide is added. When patients progress, further treatment with hormonal agents is often attempted. Some patients who have progressed after androgen deprivation do wish to receive chemotherapy. “Zytiga could prevent patients with known castration–resistant, metastatic prostate cancer from getting chemotherapy for quite a while,” Dr Bill Hait, Global Head, Janssen Research and Development and Head of the firm’s Oncology Therapeutic Area, proposed.
During an interim analysis, the independent data monitoring committee advised that the study be closed prematurely because of the benefits seen in the Zytiga arm.
“There were remarkable improvements in measurements of clinical benefits, including progression-free survival, time to chemotherapy and opiate use,” said Dr Hait.
In terms of radiographic progression-free survival, in the control arm, the median was 8.3 months. In the Zytiga arm, the median had not yet been reached. There was at least a doubling of freedom from progression. “A 33 per cent improvement has already been observed in median overall survival; in the Zytiga arm, the median still has not been reached. In the control arm, the median was 27 months,” Dr Hait said.
There are a number of other new treatments in the oncology drug development pipeline and the strategy which led to Zytiga has yielded further therapies such as Salvestrols which are also now available in Ireland.
Professor Gerry Potter the inventor of Zytiga has recently been on a lecture tour of Ireland visiting Dublin, Cork and Galway finally giving a public talk to the Ballinasloe Cancer Support Group on the discovery of Zytiga and Salvestrols. After the talk Prof Potter said "I am delighted that men in Ireland can now benefit from Zytiga and all the research that we have done. Hopefully Zytiga will be approved soon for use as an earlier treatment before chemotherapy is even needed".
Medical professionals have hailed the news that Zytiga will soon be available in
It is the second most frequent male cancer and claims the lives of 500 men a year in Ireland alone.
There are almost 17,000 suffering with the disease at the moment and
He added: "This is great news for Irish patients and their families.
"Up to now there has been no active treatment available for patients with advanced prostate cancer whose cancer has progressed after chemotherapy so this new treatment represents a real un-met clinical need." The drug will be reimbursed by health authorities here from December 1. John Dowling from the Men Against Cancer said it will give patients precious months more to live.
He added: "Men with advanced prostate cancer, if suitable, may now be offered treatment with abiraterone which may give them the real prospect of precious additional months over current treatments together with a reasonable quality of life."
“As of this moment, abiraterone acetate is not available to patients in
The drug is currently licensed for more advanced patients, who have already received chemotherapy. Its manufacturer, Janssen, is currently in talks with the National Cancer Control Programme on reimbursement for patients, similar to those in the 301 Study.
Shows great promise
Dr McDermott said: “This is an oral agent which shows great promise for patients with advanced prostate cancer, is well tolerated and improves quality of life.”
In addition, an application to the EMA’s Committee for Medicinal Products for Human Use (CHMP) is intended to extend the use of abiraterone acetate administered with prednisone for the treatment of patients with mCRPC who are asymptomatic or mildly symptomatic, after failure of androgen deprivation therapy and before chemotherapy.
Submissions have been made, based on Phase III results, which show “significant improvement” in radiographic progression-free survival and a trend for increased overall survival in patients receiving Zytiga plus prednisone.
The COU-AA-302 trial (the ‘302 Study’) was for patients who had progressed on androgen deprivation therapies but had not yet received chemotherapy.
This study, which included 1,088 asymptomatic or mildly symptomatic men with mCRPC who had not received chemotherapy, evaluated the effect of abiraterone acetate plus prednisone on the co-primary endpoints of radiographic progression-free survival (rPFS) and overall survival (OS) compared to placebo plus prednisone. Data from this study were presented at the 48th Annual Meeting of the American Society of Clinical Oncology (ASCO).
The study was designed with patients in mind who had progressed after standard androgen deprivation therapy. In most parts of the world, this involves either medical (with LHRH agonists) or surgical castration.
Often, an anti-androgen such as bicalutamide is added. When patients progress, further treatment with hormonal agents is often attempted. Some patients who have progressed after androgen deprivation do wish to receive chemotherapy. “Zytiga could prevent patients with known castration–resistant, metastatic prostate cancer from getting chemotherapy for quite a while,” Dr Bill Hait, Global Head, Janssen Research and Development and Head of the firm’s Oncology Therapeutic Area, proposed.
During an interim analysis, the independent data monitoring committee advised that the study be closed prematurely because of the benefits seen in the Zytiga arm.
“There were remarkable improvements in measurements of clinical benefits, including progression-free survival, time to chemotherapy and opiate use,” said Dr Hait.
In terms of radiographic progression-free survival, in the control arm, the median was 8.3 months. In the Zytiga arm, the median had not yet been reached. There was at least a doubling of freedom from progression. “A 33 per cent improvement has already been observed in median overall survival; in the Zytiga arm, the median still has not been reached. In the control arm, the median was 27 months,” Dr Hait said.
There are a number of other new treatments in the oncology drug development pipeline and the strategy which led to Zytiga has yielded further therapies such as Salvestrols which are also now available in Ireland.
Thursday, 15 November 2012
AT-13387 Zytiga Combo
AT-13387 is a novel inhibitor of HSP-90 a chaperone protein which stabilises a number of cellular proteins including the androgen receptor (AR). Upon HSP-90 inhibition the AR undergoes decomposition and cannot function in cell signalling. This interuption of AR stimulated signal transduction results in the death of prostate cancer cells and so HSP-90 inhibitors have therapeutic potential in the treatment of prostate cancer.
Zytiga is now widely used in prostate cancer therapy and a combination trial of AT-13387 with Zytiga is currently underway. AT-13387 is produced by Astex Therapeutics a forward looking new enterprise in oncology with several exciting new lead compounds with promising preclinical anticancer activity. The combination of AT-13387 offers a two pronged approach at blocking androgen receptor mediated prostate cancer growth and should work very well together.
Molecular structure of AT-13387 shows a cresol group which mimics the natural HSP-90 inhibitor salvestrol Q40.
Studies have shown that HSP-90 inhibition with salvestrol Q40 results in degradation of important signal transduction proteins such as the STAT kinases that ultimately leads to apoptosis and cancer cell death. Molecular modelling studies show that salvestrol Q40 inhibits HSP-90 by neatly locking in to the ATP binding site. Therefore HSP-90 inhibitors have promising potential for the treatment of a variety of cancers including prostate cancer and trials of HSP-90 inhibitors against breast cancer also look promising.
Zytiga is now widely used in prostate cancer therapy and a combination trial of AT-13387 with Zytiga is currently underway. AT-13387 is produced by Astex Therapeutics a forward looking new enterprise in oncology with several exciting new lead compounds with promising preclinical anticancer activity. The combination of AT-13387 offers a two pronged approach at blocking androgen receptor mediated prostate cancer growth and should work very well together.
Molecular structure of AT-13387 shows a cresol group which mimics the natural HSP-90 inhibitor salvestrol Q40.
Studies have shown that HSP-90 inhibition with salvestrol Q40 results in degradation of important signal transduction proteins such as the STAT kinases that ultimately leads to apoptosis and cancer cell death. Molecular modelling studies show that salvestrol Q40 inhibits HSP-90 by neatly locking in to the ATP binding site. Therefore HSP-90 inhibitors have promising potential for the treatment of a variety of cancers including prostate cancer and trials of HSP-90 inhibitors against breast cancer also look promising.
Tuesday, 13 November 2012
Importance of PI3K Signalling in Prostate Cancer
Inhibition of the PI3K pathway is an important therapeutic approach for the treatment of prostate cancer. Signalling by the PI3K/Akt/mTOR pathway plays an important role in the survival mechanism of prostate tumours and it is this signalling that is keeping the prostate cancer cells alive. Inhibit this pathway and the cancer cells automatically undergo apoptosis which is programmed cell death. It has been shown that the natural PI3K inhibitor salvestrol Q40 results in reduced downstream phosphorylation of Bcl-2 causing elevated Bax to Bcl-2 ratios that result in apoptosis. Furthermore Zytiga drug resistance pathways are mediated by the PI3K pathway and so inhibitors of PI3K such as salvestrols can be used to overcome Zytiga resistance. A number of different PI3K inhibitors are under clinical investigation in combination with Zytiga.
PI3K Signalling Pathway in Prostate Cancer
Prostate cancer is the second highest cause of male cancer related mortality. Currently the main aim of therapy for localised and metastatic disease is total androgen blockade. This aim has been achieved with Zytiga which inhibits all androgen production, thereby reducing stimulation of the androgen receptor (AR). This in turn prevents the activation of androgen-regulated genes, which normally result in on-going growth and survival of particular interest in this survival mechanism is the continued signalling by the PI3K pathway. Inhibition of testicular androgen production may be achieved surgically (bilateral orchidectomy) or chemically, using LHRH agonists. The latter induces castrate levels of testosterone by down-regulating pituitary LHRH receptors (and therefore gonadotropin hormone production) through constant stimulation. The action of androgen may be blocked at a peripheral level using anti androgens such as Casodex and Enzalutamide, which inhibit ligand binding to AR and subsequent activation. Although this approach has initial responses the majority of men relapse with castrate resistant prostate cancer (CRPC) and this is the cause of significant morbidity and mortality. To overcome this and to improve patients treatment options the mechanisms of castrate resistance need to be addressed.
The PI3K/Akt cascade regulates several cellular processes such as proliferation and apoptosis. Akt activation results in phosphorylation of multiple substrates and has been implicated in prostate carcinogenesis and castration resistance. Research has suggested that Akt interacts with signalling cascades implemented in carcinogenesis, in particular the NFkB cascade and AR signalling. The current study investigated the hypothesis that the expression and activation of PI3K/Akt cascade influences the progression to castrate resistant disease using clinical prostate cancer tumours. Fluorescent insitu hybridisation and Immunohistochemistry revealed that PTEN deletion was a common event in castrate resistant prostate cancer and low PTEN protein expression was significantly associated with a poor outcome. PTEN negatively regulates PI3K signalling. Consequently increased levels of PI3K and activated Akt (pAkt ser 308 and pAkt ser 473) were significantly associated with a shorter time to biochemical relapse and shorter disease specific survival. Inhibition of PI3K resulted in a significant reduction in cellular proliferation and Akt phosphorylation. The downstream affects of Akt activation were investigated. Akt has been reported to activate the NFkB signalling cascade both directly and indirectly.
Having shown a significant link between expression and activation of the PI3K cascade and progression to castrate resistant disease, the interaction between Akt and the AR was investigated in both clinical prostate tumours and cell lines. The phosphorylation of AR at the Akt consensus site serine 213 (pARser213) was significantly associated with disease progression. Patients with high expression pARser213 had a significantly shorter time to death from relapse and disease specific survival. Additionally 42% of patients displayed an increase in pARser213 expression, these patients also had a significantly shorter time to death from relapse and disease specific survival. Inhibition of PI3K resulted in a reduction of pARser213 expression in both cell lines. This research highlights the impact of both the PI3K/Akt and NFkB signallingcascades on prostate cancer progression and development of castrate resistant disease. In particular this study highlights the impact of Akt phosphorylation in castrate resistant prostate cancer patients. Therefore phosphorylation of AR at serine 213 may serve as a diagnostic tool to predict patient outcome in response to maximum androgen blockade and inhibition of AR 213 phosphorylation via the Akt cascade may be an effective therapeutic avenue to investigate for treatment of prostate cancer. In conclusion inhibition of the PI3K pathway can lead to cancer cell death and therefore has promising therapeutic potential. Inhibition of the PI3K pathway with natural molecules such as salvestrol Q40 and wortmanin has been demonstrated to lead directly to programmed cell death (i.e. apoptosis) of cancer cells leading to regression of primary tumours and metastases in cancer patients. In some cases complete resolution of bone metastases have been reported with these agents.
Having shown a significant link between expression and activation of the PI3K cascade and progression to castrate resistant disease, the interaction between Akt and the AR was investigated in both clinical prostate tumours and cell lines. The phosphorylation of AR at the Akt consensus site serine 213 (pARser213) was significantly associated with disease progression. Patients with high expression pARser213 had a significantly shorter time to death from relapse and disease specific survival. Additionally 42% of patients displayed an increase in pARser213 expression, these patients also had a significantly shorter time to death from relapse and disease specific survival. Inhibition of PI3K resulted in a reduction of pARser213 expression in both cell lines. This research highlights the impact of both the PI3K/Akt and NFkB signallingcascades on prostate cancer progression and development of castrate resistant disease. In particular this study highlights the impact of Akt phosphorylation in castrate resistant prostate cancer patients. Therefore phosphorylation of AR at serine 213 may serve as a diagnostic tool to predict patient outcome in response to maximum androgen blockade and inhibition of AR 213 phosphorylation via the Akt cascade may be an effective therapeutic avenue to investigate for treatment of prostate cancer. In conclusion inhibition of the PI3K pathway can lead to cancer cell death and therefore has promising therapeutic potential. Inhibition of the PI3K pathway with natural molecules such as salvestrol Q40 and wortmanin has been demonstrated to lead directly to programmed cell death (i.e. apoptosis) of cancer cells leading to regression of primary tumours and metastases in cancer patients. In some cases complete resolution of bone metastases have been reported with these agents.
BEZ-235 Zytiga Combo
BEZ-235 is a potent inhibitor of PI3K and mTOR which are involved in drug resistance. Continued AR signalling in prostate cancer is mediated by the PI3K/Akt/mTOR pathway and so inhibition of members of this pathway interferes with cell survival signalling and inhibitors of PI3K such as salvestrols causes tumours to undergo apoptosis and cell death. Zytiga resistance is believed to be mediated by PI3K signalling and various inhibitors of this pathway are under investigation in combination with Zytiga. The combination of BEZ-235 with Zytiga is being clinically trialed and should overcome drug resistance and may offer additional anticancer activity.
Molecular structure of BEZ-235 shows it is an imidazoquinoline.
Molecular structure of BEZ-235 shows it is an imidazoquinoline.
OGX-427 Zytiga Combo
OGX-427 is an antisense oligonucleotide that inhibits HSP-27 production and this new drug is being trialed in combination with Zytiga. Antisense oligonucleotides are space age technology that directly silence specific regions of DNA. In this way the technology can in principle be applied to silencing any protein of choice. This drug targets inhibition of production of HSP-27 a chaperone protein involved in the function of other important kinase enzymes involved in tumour cell proliferation. However there are many unanswered questions with regards to the antisense oligonucleotide approach in general, such as its efficacy and toxicity. Moreover the benefits of HSP-27 inhibition in the treatment of cancer have not been proven and the results of this clinical trial will be interesting.
Sunday, 11 November 2012
USA Leads the Way in Prostate Cancer Therapy With Zytiga
The USA leads the way in using cutting edge drugs in clinical practise and Zytiga is now beeing used in 48% of prostate cancer patients in the USA who have progressed following chemotherapy. The use of Zytiga before chemotherapy is less frequent since it has not yet been FDA approved in this scenario. Zytiga has a lot of advantages over other options such as chemotherapy and its approval before chemotherapy by the FDA is being fast tracked with an announcement expected in December.
The abiraterone.blogspot website was set up to give as much information as possible to prostate cancer sufferers about abiraterone acetate (Zytiga) which is a promising new treatment for prostate cancer. This blog also strives to give up to the minute information on other new treatment options for prostate cancer and information on new drugs as they emerge. Regular updates on feeback from patients taking Zytiga are included together with news on new Zytiga combinations with promising potential. This information has been most widely viewed in the USA and the UK with viewers also coming from India and the Ukraine.
abiraterone.blogspot.com viewing statistics
The abiraterone.blogspot website was set up to give as much information as possible to prostate cancer sufferers about abiraterone acetate (Zytiga) which is a promising new treatment for prostate cancer. This blog also strives to give up to the minute information on other new treatment options for prostate cancer and information on new drugs as they emerge. Regular updates on feeback from patients taking Zytiga are included together with news on new Zytiga combinations with promising potential. This information has been most widely viewed in the USA and the UK with viewers also coming from India and the Ukraine.
abiraterone.blogspot.com viewing statistics
United States
|
5239
|
United Kingdom
|
1019
|
Canada
|
453
|
Germany
|
428
|
Australia
|
345
|
France
|
327
|
Russia
|
256
|
India
|
202
|
Italy
|
160
|
Ukraine
|
107
|
Saturday, 10 November 2012
Jevtana Vs Zytiga
Both Jevtana and Zytiga are licensed for use following Docetaxel chemotherapy so what does each have to offer ?
Jevtana is another form of chemotherapy and is a taxane similar to Docetaxel. Jevtana has all the side effects of chemotherapy including liver and kidney damage as well as toxicity to white blood cells causing immunosuppression. Clinical trials showed that Jevtana treatment extended life by only 2.4 months.
Jevatana (Cabazitaxel) is given as an injected infusion every three weeks in a cycle of 3 rounds of chemotherapy. Its cost is around £ 8,000 per infusion and it is not yet approved by NICE for use on the UK NHS.
Zytiga is a form of hormonal therapy that does not suffer from the side effects of chemotherapy and this is why it is the preffered treatment over Jevtana. Zytiga is taken as an oral tablet once daily and is able to work against advanced metastatic disease for which it is FDA apporved. Zytiga is also approved for use on the NHS in the UK.
Jevtana is another form of chemotherapy and is a taxane similar to Docetaxel. Jevtana has all the side effects of chemotherapy including liver and kidney damage as well as toxicity to white blood cells causing immunosuppression. Clinical trials showed that Jevtana treatment extended life by only 2.4 months.
Zytiga is a form of hormonal therapy that does not suffer from the side effects of chemotherapy and this is why it is the preffered treatment over Jevtana. Zytiga is taken as an oral tablet once daily and is able to work against advanced metastatic disease for which it is FDA apporved. Zytiga is also approved for use on the NHS in the UK.
Wednesday, 7 November 2012
Stelara Shines in Trials
Stelara the new treatment for Psoriasis has succesfully completed clinical trials and has now been licensed and FDA approved for the treatment of acute psoriasis. Stelara is a monoclonal antibody therapy which is given as a monthly 45 mg subcutaneous injection. The ACCEPT clinical trials showed that Stelara (aka Ustekinumab) effectively treated psoriasis with minimal side effects. Stelara has been designed as a very selective form of therapy specifically targetting IL-12 which is involved in psoriasis plaque formation. By selectively targetting IL-12 Stelara is able to exert its effects aginst psoriasis withou causing any other side effects.
Stelara, Zytiga, and Xarelto are 3 new bockbuster drugs from health giant Johnson & Johnson who know a good drug when they see one, and have selected key drugs in there respective clinical settings. Stelara has unique activity against psoriasis, Zytiga is highly effective against advanced prostate cancer, and Xarelto is an effective anticoagulant used to prevent strokes.
Stelara, Zytiga, and Xarelto are 3 new bockbuster drugs from health giant Johnson & Johnson who know a good drug when they see one, and have selected key drugs in there respective clinical settings. Stelara has unique activity against psoriasis, Zytiga is highly effective against advanced prostate cancer, and Xarelto is an effective anticoagulant used to prevent strokes.
Tuesday, 6 November 2012
Xarelto Receives FDA Approval
Xarelto the new potential blockbuster by Zytiga manufaturers Johnson & Johnson has received FDA approval for treating variuos types of heart disease and cardiovascular disorders. These include treatment and prohylaxis of AtrialFibrillation, Stroke, and Deep Vein Thrombosis (DVT). Xarelto is the trade name of the powerful anticoagulant agent Rivaroxaban which is an inhibitor of blood clotting factor X alpha. It has powerful anticoagulant effects and prevents blood clots from forming. It is effective at a very low dose of only 10 mg daily taken orally so it is a very convenient and effective means for preventing conditions where blood clots cause problems such as stroke and deep vein thrombosis.
Johnson & Johnson really are on to two winners here producing both Zytiga and Xarelto. It may be that some people need to take both Zytiga and Xarelto together for example patients with advanced metastatic prostate cancer that are also suffering form atrial fibrillation or are at risk of stroke. So these medications may well be used in the same patient populations and these 2 drugs should work well together. The best timing would be to take the Zytiga dose first thing in the morning with 5 mg prednsione, and then 4 hours later to take 10 mg of the Xarelto and the other 5 mg of prednisone. This way there will be minimal pharmacological reactions between the 2 drugs. Both drugs are cleared from the body by the enzyme CYP3A4 and so will compete for this enzyme which will extend the half lives of both these compounds. By offsetting the dosing schedule the competition for CYP3A4 will be reduced and both drugs metabolised safely.
Johnson & Johnson really are on to two winners here producing both Zytiga and Xarelto. It may be that some people need to take both Zytiga and Xarelto together for example patients with advanced metastatic prostate cancer that are also suffering form atrial fibrillation or are at risk of stroke. So these medications may well be used in the same patient populations and these 2 drugs should work well together. The best timing would be to take the Zytiga dose first thing in the morning with 5 mg prednsione, and then 4 hours later to take 10 mg of the Xarelto and the other 5 mg of prednisone. This way there will be minimal pharmacological reactions between the 2 drugs. Both drugs are cleared from the body by the enzyme CYP3A4 and so will compete for this enzyme which will extend the half lives of both these compounds. By offsetting the dosing schedule the competition for CYP3A4 will be reduced and both drugs metabolised safely.
Sunday, 4 November 2012
Zytiga Required Before Xtandi Insurance Cover
Insurance companies in the US are only covering Xtandi for use after Zytiga therapy has failed. This clause for the use of Xtandi requires prior use of Zytiga and have clinically progressed on this treatment. Only then will the insurance companies cover the use of Xtandi. This is probably because Xtandi costs $7,500 per month which is considerably more than Zytiga at $5,000 per month.
However there is no clinicall evidence so far that Xtandi works in Zytiga relapsed patients. Patients who have Zytiga Resistant Prostate Cancer (ZRPC) have tumours that have become completely hormone independent so they are unlikely to respond to another antihormonal therapy such as Xtandi. Zytiga has been shown to work when Xtandi has failed but there is currently no evidence that Xtandi will work when Zytiga has failed.
The trial of the closely related antiandrogen AR-509 shows hope that Xtandi may show reponses after Zytiga, since AR-509 is a closely related analogue of Xtandi, and the clinical trials on AR-509 showed a 10% response rate in prostate cancer patients who had previously received Zytiga. So there is hope that at least some patients may benefit from Xtandi post Zytiga.
However there is no clinicall evidence so far that Xtandi works in Zytiga relapsed patients. Patients who have Zytiga Resistant Prostate Cancer (ZRPC) have tumours that have become completely hormone independent so they are unlikely to respond to another antihormonal therapy such as Xtandi. Zytiga has been shown to work when Xtandi has failed but there is currently no evidence that Xtandi will work when Zytiga has failed.
The trial of the closely related antiandrogen AR-509 shows hope that Xtandi may show reponses after Zytiga, since AR-509 is a closely related analogue of Xtandi, and the clinical trials on AR-509 showed a 10% response rate in prostate cancer patients who had previously received Zytiga. So there is hope that at least some patients may benefit from Xtandi post Zytiga.
Saturday, 3 November 2012
Cigarette Smoking Protects Against Side Effects of Chemotherapy
Surprising new research results are showing that cigarette smokers suffer less from the side effects of chemotherapy than non-smokers. This is the first time that cigarette smoking has been shown to have positive health benefits. In particular cigarette smokers suffered less damage to the important white blood cellls. This was reflected in a decreased incidence of neutropenia among cigarette smokers. Importantly the white blood cell count (WBC) remained good in the smokers.
The reason for this effect may be due to modulation of the nicotinoid receptors ro could be due to the fact that cigarette smokers are accustomed to having toxic compounds in the body which renders them less susceptible of the toxic effects of the chemotherapy.
Maybe the effects of smoking marijuana should also be investigated on alleviating other side effects of chemotherapy in addition to its use in relieving pain as a narcotic and medical marijuana oil extracted from cannabis indica and cannabis sativa has shown remarkable anticancer properties in its own right due to the THC and CBD acting at the cannabinoid receptors. Smoking cannabis with tobacco will modulate both the cannabinoid and nicotinamide receptors and should work together to alleviate the side effects of chemotherapy.
The research results are summarised below:
The reason for this effect may be due to modulation of the nicotinoid receptors ro could be due to the fact that cigarette smokers are accustomed to having toxic compounds in the body which renders them less susceptible of the toxic effects of the chemotherapy.
Maybe the effects of smoking marijuana should also be investigated on alleviating other side effects of chemotherapy in addition to its use in relieving pain as a narcotic and medical marijuana oil extracted from cannabis indica and cannabis sativa has shown remarkable anticancer properties in its own right due to the THC and CBD acting at the cannabinoid receptors. Smoking cannabis with tobacco will modulate both the cannabinoid and nicotinamide receptors and should work together to alleviate the side effects of chemotherapy.
The research results are summarised below:
Smoking Protects Against Side Effects of Chemotherapy
Purpose:
Compounds in cigarette smoke are known to interact with the metabolism of several anticancer drugs. They may also affect the incidence and severity of adverse events and the efficacy of chemotherapy. The main objective of this study was to examine the effects of smoking tobacco on the pharmacokinetics and toxicities of patients treated with the chemotherapy agents docetaxel (Taxotere) or paclitaxel (Taxol).
Compounds in cigarette smoke are known to interact with the metabolism of several anticancer drugs. They may also affect the incidence and severity of adverse events and the efficacy of chemotherapy. The main objective of this study was to examine the effects of smoking tobacco on the pharmacokinetics and toxicities of patients treated with the chemotherapy agents docetaxel (Taxotere) or paclitaxel (Taxol).
Experimental Design:
Smoking status, toxicity profiles, and pharmacokinetic parameters were determined in 566 patients (429 nonsmokers and 137 smokers) treated with docetaxel or paclitaxel.
Smoking status, toxicity profiles, and pharmacokinetic parameters were determined in 566 patients (429 nonsmokers and 137 smokers) treated with docetaxel or paclitaxel.
Results:
Smokers treated with docetaxel showed significantly less grade IV neutropenia (35% vs. 52%) than nonsmokers. Smokers treated with paclitaxel had less grade III–IV leukopenia than nonsmokers (12% vs. 25%), and the white blood cell count (WBC) nadir was lower in nonsmokers (median, 2.7 x 109/L; range, 0.05 x 109 to 11.6 x 109/L) than in smokers (median, 3.3 x 109/L; range 0.8 x 109 to 10.2 x 109/L). Of interest, significantly lower WBC counts and absolute neutrophil counts at baseline were seen in nonsmoking patients treated with paclitaxel (P = 0.0001). Pharmacokinetic parameters were similar in smokers and nonsmokers for both taxanes.
Smokers treated with docetaxel showed significantly less grade IV neutropenia (35% vs. 52%) than nonsmokers. Smokers treated with paclitaxel had less grade III–IV leukopenia than nonsmokers (12% vs. 25%), and the white blood cell count (WBC) nadir was lower in nonsmokers (median, 2.7 x 109/L; range, 0.05 x 109 to 11.6 x 109/L) than in smokers (median, 3.3 x 109/L; range 0.8 x 109 to 10.2 x 109/L). Of interest, significantly lower WBC counts and absolute neutrophil counts at baseline were seen in nonsmoking patients treated with paclitaxel (P = 0.0001). Pharmacokinetic parameters were similar in smokers and nonsmokers for both taxanes.
Conclusion:
Cigarette smoking does not hinder the action of docetaxel and paclitaxel. Cigarette smokers treated with the chemotherapy agents docetaxel and paclitaxel had significantly less side effects of neutropenia and leukopenia, and further research is warranted to elucidate this potential protective effect.
Cigarette smoking does not hinder the action of docetaxel and paclitaxel. Cigarette smokers treated with the chemotherapy agents docetaxel and paclitaxel had significantly less side effects of neutropenia and leukopenia, and further research is warranted to elucidate this potential protective effect.
Friday, 2 November 2012
Zytiga Inventor Receives Award from Canada
The inventor of Zytiga Professor Gerry Potter has received an award from Canadian cancer diagnostics company CARE Biotechnologies. Zytiga is now approved by Health Canada and is now available in Canadian pharmacies. It is licensed for post chemotherapy use after the drug docetaxel has failed. Professor Potter said on receiving the award "It is so frustarting that Zytiga is not licensed before chemotherapy afterall it is a far safer drug and should be used before chemotherapy is even thought of. Chemotherapy should be alast ditch event after Zytiga has failed not the other way round. Its about time that the FDA approved Zytiga before chemotherapy so that many more men can benefit from this treatment. I designed this drug to replace chemotherapy which is an outdated form of cancer treatment that causes serious side effects. Docetaxel is toxic to the liver, kidneys, and white blood cells so causes severe immunosuppresion. This is not good depleting the cancer patients immune system destrying the very cells that help in cancer recovery. So it really is a nonsense using those sorts of chemotherapy and its about time we abandoned that approach completely. Zytiga makes chemotherapy obsolete and so of course it should really be used as a first line therapy. I'm very please this drug is now benefiting prostate cancer patients in Canada"
Professsor Dan Burke made the award on behalf of CARE biotech, a company specialising in proteomic approaches to early cancer detection that resulted as a spin out from Professor Potter's research on the CYP1B1 and CYP17 enzymes.
www.IJOPT.org
Professsor Dan Burke made the award on behalf of CARE biotech, a company specialising in proteomic approaches to early cancer detection that resulted as a spin out from Professor Potter's research on the CYP1B1 and CYP17 enzymes.
www.IJOPT.org
Subscribe to:
Posts (Atom)