Homocysteine can be lowered by supplementing with vitamins B12, B6, and folic acid.

In order for folic acid to remove homocysteine, it first must be converted to its active form called L-methylfolate (5-MTHF). The diagram to the right shows the steps required in the body to convert folic acid to metabolically active L-methylfolate:

The conversion steps needed to form 5-MTHF outlined on the previous page require specific enzymes that in some people are impaired since birth. In other individuals, the activity of these enzymes slows with aging, which helps explain why homocysteine levels so often surge in the elderly.

Fortunately, we don’t have to rely on a perfect sequence of enzymes in our body to lower homocysteine. By taking L-methylfolate (also known as 5-methyltetrahydrofolate or 5-MTHF) directly, we can confidently lower homocysteine.

Published studies show that 5-MTHF achieves higher blood levels of active folate^1,2-and more importantly, lowers homocysteine³ and extends survival in human study subjects.⁴

When was the last time you or your doctor checked your homocysteine levels? Can’t remember? Never? Either of these answers puts you at risk of a silent killer.^5-7

Conventional doctors rarely test their patients' homocysteine levels. Yet a low-cost blood test quickly reveals if you are in a danger zone.^8,9

Most doctors don't test for it and certainly don’t know how easy it is to treat high homocysteine with a unique form of folate known as 5-MTHF.

Devastating Impact Of High Homocysteine

Elevated homocysteine levels (hyperhomocysteinemia) are an important, independent risk factor for cardiovascular diseases including atherosclerosis and its consequences, heart attack, stroke,^10,11and peripheral vascular disease.^5,12,13

Homocysteine is an amino acid that’s very similar to the amino acids used by the body to make proteins.¹⁴But, unlike these beneficial amino acids, homocysteine has toxic properties that contribute to poor health.^15,16 High levels of homocysteine have been associated with numerous degenerative diseases.¹⁴

According to one study, 42% of patients with cerebrovascular disease (stroke or near stroke) had hyperhomocysteinemia, 28% of those with peripheral vascular disease (obstruction of blood vessels, especially in the legs) had elevated levels, and 30% of those with coronary artery disease (obstruction of the heart’s own blood supply, the coronary arteries) had elevated homocysteine levels.¹⁷

In a recent study of patients who had survived a heart attack, researchers divided over 800 subjects into two groups-those with high plasma homocysteine (defined as greater than 15 micromol/L in the study) and those with lower levels.⁵

After just 30 days, researchers found the rates of complications such as heart failure, heart rupture, death, and total adverse cardiovascular events were significantly higher in the elevated homocysteine group compared with those in the group with lower levels. Again, the higher the homocysteine level, the greater the incidence of adverse cardiovascular events.

Why Homocysteine Is So Dangerous

Scientists are still investigating the exact mechanism as to why homocysteine contributes to these grave health risks, but several convincing mechanisms are emerging. The most prominent ones involve homocysteine’s ability to elevate oxidant stress, alter lipid (fat) metabolism, and promote excessive blood clotting.¹⁸

Recently, links have been established between homocysteine and vital signaling information used by arteries to control blood pressure.^19-21 There’s also evidence that homocysteine has damaging effects on the HDL-associated enzyme paraoxonase1, or PON1, which is required to protect LDL from oxidation.^18,22-24

It is now clear that rising homocysteine levels are significantly associated with threats to the cardiovascular system, particularly to the aging adult. Mainstream medicine often ignores this information,^25-27 and frequently offers little or no help to lower deadly homocysteine levels in patients.

What you need to know: Lower Homocysteine With High-Potency Folate

• A high level of the amino acid homocysteine is a strong predictor of cardiovascular diseases such as heart attack and stroke, the leading killers of Americans.
• Folic acid supplementation is recommended as part of a B-vitamin package aimed at reducing homocysteine levels.
• But many people find their homocysteine levels stubbornly resist even high doses of folic acid.
• Such people may carry a gene variant that weakens their ability to generate the active form of folate, called 5-MTHF, resulting in elevated homocysteine levels.
• Supplementing directly with 5-MTHF evades the decrease in enzyme activity because it requires no further metabolism to achieve homocysteine-lowering effects.
• Get your homocysteine levels checked at least annually; if your levels resist therapy with standard folic acid, you should switch to the active, 5-MTHF form.

In the body, the folate molecule goes through several enzymatic steps to become the active molecule 5-MTHF.^28-30 It is the active 5-MTHF form of folate that participates in the homocysteine-lowering step that results in the production of the safe amino acid, methionine.^28,30

It makes sense, then, that low levels of folate are predictive of elevated homocysteine levels.³¹

In theory, supplementing with folic acid-the most common form of folate in supplement form-should provide the body with the folate it needs to convert dangerous homocysteine into safe methionine. Unfortunately, this readily available homocysteine-lowering regimen doesn’t work for everyone.

That’s because in order to make the conversion from folate to the active 5-MTHF, an enzyme called methylenetetrahydrofolate reductase or MTHFR is necessary-and not everyone carries the same version of this important enzyme. It is estimated that between 5 and 10% of the population has a gene variant that reduces MTHFR activity by 70%,³²while nearly 50% of people of European descent have a genetic variation that decreases MTHFR activity by as much as 35%.^28,29,33-36

If you fall into these categories, you are likely to be a victim of persistently high homocysteine levels-even if you are taking high doses of folic acid.³⁷

The solution is simple: Instead of relying only on the folic acid in your multinutrient formula, supplement with 5-MTHF. By doing this, you’ll bypass the enzyme defect and provide your body with exactly the right molecule it needs to begin lowering those dangerous homocysteine levels.³⁸

A wealth of laboratory and human studies demonstrate that 5-MTHF is the best form of folate required for lowering dangerous homocysteine levels.

5-MTHF: More Effective Than Folic Acid

Numerous animal and human studies have proven that 5-MTHF is more effective than folic acid at increasing serum active folate levels.

In a compelling animal study, mice were bred to have two copies of the defective gene for MTHFR, the enzyme involved in making 5-MTHF, which in turn, converts homocysteine into methionine.³⁹The animals had markedly elevated homocysteine levels as a result, and almost all died in infancy from homocysteine toxicity.

However, when their mothers (who survived because they carried one normal and one abnormal gene) were fed 5-MTHF during pregnancy, 64% of the offspring survived, compared with the 95% mortality rate seen in pups of mothers supplemented with folic acid. Encouragingly, the pups from mothers supplemented with 5-MTHF also showed improved appearance of structures in their brains that were previously affected by folate deficiency.

Human studies validate the superiority of 5-MTHF over folic acid.

One crossover study evaluated cardiovascular patients known to have two copies of the gene for the weakened MTHFR enzyme.³⁸Subjects received a single 5 mg oral dose of either folic acid or 5-MTHF, and then after a washout period, each patient received the opposite supplement from what they originally received. Researchers found that the subjects' peak serum folate levels were nearly 7 times higher when taking the active 5-MTHF as they were when they took the folic acid supplement, demonstrating superior bioavailability of the 5-MTHF form.

Another crossover study involved a group of healthy women, one-third of whom had the typical gene variant for MTHFR, and two-thirds of whom had the weaker gene variant.³⁵Each woman received either 400 mcg of folic acid or 416 mcg of 5-MTHF. (The slightly higher dose in micrograms reflects chemical differences between folic acid and 5-MTHF; it represents the same dose of folate at the cellular level.) After the first phase of the study, the dosing regimen was reversed, and each woman received the opposite supplement from the first.

Regardless of the women’s genetic makeup, the total amount of folate in blood, as well as the maximum concentration reached, were significantly higher when the women were taking 5-MTHF compared to when they were taking folic acid.³⁵

5-MTHF Lowers Homocysteine Levels

The superiority of 5-MTHF for increasing blood levels of folate directly translates to lower homocysteine levels.

This was first shown in a study of healthy people.⁴⁰For the study, a low dose of 5-MTHF (113 mcg per day) was compared with a low dose of folic acid (100 mcg per day). After six months, the mean total homocysteine was reduced by 14.6% in the 5-MTHF group, compared with only 9.3% in the folic acid group.

Further support for the superiority of 5-MTHF as a homocysteine-lowering supplement comes from a study of patients with kidney disease on dialysis.⁴ This group of people is at very high risk for elevated homocysteine levels,^41,42as well as high rates of complications and cardiovascular disease that occur as a result. In fact, 93% of this group of people had homocysteine levels above the upper limit of normal, which is considered in this study to be 12 micromol/L.

Subjects were divided into two treatment groups: The first one received 50 mg of intravenous 5-MTHF at the end of each dialysis section and the second received 5 mg per day of folic acid, orally. Both groups received the same intravenous dose of vitamins B6 and B12. After six months, homocysteine levels were reduced to an average of 20.7 micromol/L in the 5-MTHF group, compared with stubbornly high levels of 35.0 micromol/L in the folic acid group.⁴Along with the greater homocysteine reduction, after 24 months, those in the 5-MTHF group also had significantly lower levels of the inflammatory marker C-reactive protein, or CRP.

Most importantly, however, was the impact 5-MTHF had on survival. Subjects in the 5-MTHF group survived on average 36.2 months after beginning treatment, while those in the folic acid group survived an average of only 26.1 months-that’s a 39% increase in survival in the 5-MTHF group!⁴ Interestingly, the doctors who conducted this study attributed the improved survival on the reduction in CRP observed in the 5-MTHF group.

5-MTHF And Depression

5-MTHF is clearly a superior way to achieve optimal blood levels of active folate, as well as the best means known for lowering dangerous homocysteine levels. But it has other benefits as well. Because folate is required in processes that produce the brain’s neurotransmitters,⁴³5-MTHF has also attracted the interest of researchers that investigate major depression, a condition that reflects imbalances in neurotransmitter quantity or effect.⁴⁴

Major depression is a debilitating illness that is very difficult to treat: Only about 30% of patients treated with a single antidepressant drug achieve remission of their symptoms, a figure that only rises to 50 to 55% when a second drug is added.^45,46 As a result, there has been a major push to find non-pharmacological therapies that could improve response rates. Once researchers discovered that people with low serum and red blood cell levels of folate have poorer responses to antidepressant therapy, they decided to see if adding 5-MTHF to antidepressant drugs could improve response rates.⁴⁵ The results have been dramatic.

In one study, 19% of patients taking 5-MTHF plus a regular antidepressant drug experienced major improvement on a standard depression score, compared with just 7% of those who only took an antidepressant drug.⁴⁷That response rate was even higher among patients with the worst degree of impairment from depression, with 40% of those taking 5-MTHF in addition to their regular antidepressants experiencing major improvement versus just 16% of those taking antidepressants only.

In addition, the 5-MTHF group experienced these improvements significantly faster than the control group-in 177 days versus 231 days. Once again, those with the most severe depression experienced the most dramatic results, with the median time to improvement in the 5-MTHF group being 85 days, compared with 150 days in control subjects. Impressively, nearly twice as many people in the antidepressant-only group stopped therapy because of adverse events (34%) versus the 5-MTHF group (17.9%), a testament to the supplement’s safety.

Numerous other studies have achieved similar results when 5-MTHF is added to a standard antidepressant drug; doses used are typically 15 mg day.^48-50An abnormal gene variant for 5-MTHF synthesis and metabolism may predict resistance to antidepressant therapy and help identify patients who may be responsive to adjunctive therapy with 5-MTHF.⁵¹

5-MTHF And Diabetic Peripheral Neuropathy

Diabetic peripheral neuropathy is another condition that reflects imbalances in neurotransmitter quantity or effect,⁵²leading researchers to investigate 5-MTHF as a potential treatment. Diabetic peripheral neuropathy is a painful condition that causes slowing and abnormal transmission of nerve impulses,⁵³which results in both pain and loss of sensitivity to normal touch.⁵⁴

The combination of 5-MTHF with vitamin B12 (methylcobalamin) and an active form of vitamin B6 (pyridoxal-5’-phosphate) has been used to treat endothelial dysfunction, and is now under active exploration for use in diabetic neuropathy.

An animal study showed that this combination, at a human equivalent dose, increased the density of nerve fibers in the skin and improved nerve sensory conduction and responses to temperature and mechanical touch.⁵⁵These improvements occurred in the absence of changes in blood sugar.

Studies have shown that when humans with diabetic peripheral neuropathy are treated with this supplement combination, they experience improvements of skin sensitivity to touch and reduction in painful symptoms.^56,57 One such trial also showed improvements in the density of nerve fibers in the skin,⁵⁷and a different trial also noted a significant decrease in homocysteine levels compared with a small increase in placebo recipients.⁵⁶

Testing For Homocysteine

Your homocysteine levels can be determined by a simple blood test. Knowing your homocysteine status will allow you take therapeutic action if your levels are too high. Remember to fast for eight to 12 hours before the blood test. Do not eat any food or drink liquids other than water before the test and take any medications as prescribed. Do not take your supplements the morning of the test.

Summary

High levels of the amino acid homocysteine are a major threat to an aging person’s health, raising the risk for cardiovascular disorders such as heart attack and stroke. Folate is known to be effective in lowering homocysteine levels, but a large proportion of people find that their homocysteine levels remain stubbornly high, even on folic acid supplements.

This could be caused by the fact that 5 to 10% of the population and nearly half of people of European descent carry a gene variant that reduces the activity of the enzyme required to efficiently convert folic acid into the active, homocysteine-lowering form of the vitamin, 5-MTHF.

For people with persistently high homocysteine levels, high-dose 5-MTHF is now available as a supplement.

Published studies show that 5-MTHF not only lowers homocysteine and CRP, but also improves human survival.

If your homocysteine-lowering regimen seems stalled, don’t simply raise your dose of folic acid. Instead, switch to 5-MTHF, the active form of the supplement. Then test your homocysteine levels again in 30 days to ensure you are taking the proper dose of 5-MTHF. Some people with high homocysteine may only need 5 mg (5,000 mcg) of 5-MTHF once daily while others will need to take 5 mg of 5-MTHF twice a day.

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...

With spurious liquor claiming at least 104 lives in Malwani, it has emerged as the city’s worst hooch tragedy. However, it now seems that the lethal liquor might have taken a greater toll because many of the patients at a BMC-run hospital did not receive timely dialysis, required to flush out toxic methanol from their bodies.

Mumbai liquor tragedy: CM wants death penalty for Malwani hooch culprits

Most of the victims of the Malwani hooch tragedy suffered kidney failure, as a direct result of methanol intake, and were in dire need of dialysis

As the deadly hooch began taking effect around 8.30 pm on Thursday evening, a majority of the patients as many as 139 were rushed to Shatabdi Hospital in Kandivli, which is one of the largest public medical facilities in the vicinity. Despite its scale, however, Shatabdi is a secondary care centre and lacks a dedicated nephrology, plastic surgery or neurosurgery department.

Mumbai liquor tragedy: 5 more families say hooch killed their loved ones, cops blame it on illness

A family member performs the last rites of one of the victims of the Malwani hooch tragedy at a crematorium in Malad. Having claimed 104 lives, this counts as the worst hooch  tragedy in the city

Instead, the dialysis centre there is run by the private trust, Naminath Jain Foundation under a public-private partnership. However, the centre had already shut by 5 pm, and was not reopened despite the dire need of the hooch patients. Many of the patients were in need of dialysis, but not all were medically fit to be moved to other hospitals.

Even those who were, had to wait at least five to six hours before they could be transferred and complete the whole documentation process. The numbers tell the rest of the story: within 24 hours, there were at least 50 casualties reported at Shatabdi, that has so far seen a total of 61 deaths in this case.

The hospital transferred 60 patients who were in need of dialysis or better medical facilities to KEM, Nair and Sion hospitals or other private hospitals across the city. However, doctors have indicated that many deaths could have been avoided had the patients been provided dialysis at Shatabdi itself.

But according to Dr Krishnakant Pimple, medical superintendent at Shatabdi Hospital, the private trust-run facility could only run from 9 am to 5 pm as per the contract. However, even when the dialysis centre reopened the next day (Friday), it remained busy with its own patients and did not provide treatment to the hooch patients.

“The trust-run facility had their own patients to attend to, and the hospital had no control over the facility to ask them to treat the hooch patients. The trust had 70 other patients to attend to, who are suffering from chronic kidney ailments and need dialysis twice or thrice a week,” Dr Pimple told mid-day.

The deceased victims at Shatabdi were sent for post-mortem to the Bhagwati post-mortem centre, where the chief, Dr Shivaji Kachare agreed that dialysis had an important role to play in treating the patients.
“Unlike ethanol (drinking alcohol), methanol takes time to affect the organs.

Once it changes into formic acid, it begins to affect the kidneys and liver and that’s when the patient needs to be put on dialysis and life support immediately,” he said. 27 patients were shifted to Nair Hospital, of whom 10 succumbed during treatment, while the remaining are said to be critical but stable.

“The exact cause of death is yet to be disclosed and will only be known after the chemical analysis findings from the state-run forensic laboratory. But on the other hand, we can’t deny that immediate treatment could’ve saved more lives. Methyl alcohol or methanol has direct neurological and nephrological effects, and if not attended on time, it could be fatal,” said a doctor at Nair, on the condition of anonymity.

At KEM, four out of 16 transferred patients died as they were in a critical condition, while of the remaining 12, six were put on dialysis and are now showing improvement, said the dean, Dr Avinash Supe. Similarly, according to the on-duty Assistant Medical officer (AMO) at Sion Hospital, Dr Sarita Patil, of the six transferred patients, three were in immediate need of dialysis.

Mumbai hooch tragedy: More people flock to hospitals just to be safe

The management at Shatabdi Hospital, however, maintained that none of their patients were put through any inconvenience or danger. “The claims that we could have saved more patients by offering timely dialysis but we delayed it, are totally false. Whoever needed dialysis was moved to other hospitals,” said medical superintendent Dr Pimple.

The Other Side
When mid-day approached BMC Additional Commissioner (Health) Sanjay Deshmukh over the issue, he said, “The dialysis centre at Shatabdi did not have a qualified nephrologist, required for haemodialysis, and hence all the patients who needed dialysis support had to be shifted to other hospitals, as it would have been a waste of time to wait for a consulting nephrologist to visit the hospital.”

But while Deshmukh seemed to think the centre did not have a nephrologist, one of the trustees from the facility, Bipin Sanghvi said, “We have a qualified nephrologist who even does haemodialysis.” Asked whether the trust had received any request from Shatabdi Hospital to open the dialysis centre for the hooch patients, Sanghvi said, “I am not aware about it and will have to check, only after which can I comment.”

...

FRANK Baker is still determined to see a managed renal unit situated in Young.

Frank Baker speaking at last week’s Young Shire Council meeting.

FRANK Baker is still determined to see a managed renal unit situated in Young.

Mr Baker, whose late wife Helen was a renal patient, stood before Young Shire Council last week saying he felt the best approach would be through a submission to NSW Health.

“We have to make our application a needs-based application rather than a submission based on emotion,” he said.

“Decision making in health is made by the managerial staff of the health department based on the needs of the community in delivery of health, the cost of delivery and the practical implementation of such.

“Each dollar spent in health has to weigh up to deliver the best statewide system,” Mr Baker said.

He has suggested firstly presenting Young’s case to the Murrumbidgee Area Health manager, highlighting the numbers of patients presently travelling long distances for treatment and the viability of a unit in Young to meet this much-needed service.

“We then move one step further up the chain and meeting with the manager of the NSW Health unit that decides it is viable to establish this service,” he said, “again the submission has to be accurate, convincing and not purely emotional.”

Mr Baker said he understood the granting of a unit to Cowra was based on logistics, need, distance and the availability of funds to achieve the best outcome at the time.

“In the draft planning of the Murrumbidgee Area Health, Young was at the top of the list for a satellite unit managed by Wagga but in the overall picture of NSW it does not guarantee that we get the unit, it is part of the overall consideration with other area health units,” he said.

Mr Baker said when Young first started to make a move for a satellite unit 13 years ago, the town had seven patients travelling to Canberra three times a week.

He said in 2010 the estimate was that in 2016, 14 local patients would require dialysis.

“We now have only two to three travelling to Canberra,” he said.

Despite this he says Young people should coordinate their efforts to achieve the aim of having a satellite renal unit.

In response, Young’s general manager Peter Vlatko said the council was not looking to MLHD staff.

“They’ve done everything they can,” he said.

“The decision is not up to them, it is a political decision and, to that end, we have taken action,” he said, confirming Young’s mayor John Walker had requested a meeting with NSW Health Minister Jillian Skinner.

A signed petition by locals protesting the loss of the satellite renal unit will be presented at parliament tomorrow by MLC Mick Veitch,

Mr Veitch told The Witness last week the health minister is required to respond in writing to that petition.

...

LONDON, June 23, 2015 /PRNewswire/ -- There are today at least 238 targeted molecular therapies known to affect more than 240 specific intracellular signaling pathways for the treatment of renal cancer. The rational for this plethora of treatment strategies is based on our increasing understanding of the 202 drug targets that are included in this drug-pathway analyzing tool. No less than 198 of these have been recorded with mutations and 39 drug targets have mutations which have been causally implicated in cancer.

Pathway Coverage
- BioCarta# 223 Pathways
- KEGG# 185 Pathways
- NCI-Nature# 240 Pathways
- NetPath# 32 Pathways

Pipeline Coverage
Marketed# 25
Pre-registration# 1
Phase III# 12
Phase II# 79
Phase I# 68
Preclinical# 26
Suspended# 3
Ceased# 95

The continuous identification of drug targets and pathways that are altered in cancer is not only crucial for our understanding of cancer biology, but also to search for new targets for early diagnosis and improved treatment designs. Consequently, it has never before been as important to rapidly translate systems biology of disease and therapeutics to actionable pipeline decisions to ensure that the optimal market conditions exist by the time a candidate drug is commercialized.

For this reason BioSeeker, a leader in pipeline analytics, has constructed this high-level drug-pathway analyzer which lets you interact with the renal cancer pipeline in a whole different than way than you ever done before. Its capabilities moves you beyond powerful competitive intelligence to an opportunity seeking tool which lets you, by means of both present and emerging scientific knowledge, analyze the renal cancer pipeline for interesting compounds which affect and/or fit your purposes, may it be benchmarking, in/out-licensing, combination therapy options, drug repositioning, indication expansion etc.

You Use this Analyzer Tool in Renal Cancer to:

* Map the competition and find suitable benchmarking/licensing drugs based on specific pathways and drug properties

* Uncover potential indication expansion areas for your drug portfolio

* Reveal repositioning opportunities for your older, shelved drugs

* Evaluate the progression and success of targeting certain pathways by different tumor types

* Investigate drugs which affect crosstalk between key pathways

* Investigate different combination therapy options available to you in various cancer types. Use this tool to look for the most-efficient ways to combine your drug with other targeted agents.

* Find possible adjuvant therapy settings with other drugs.

This is how you do it:
In analyzing drug-pathway relationships this tool has three core modes:

1. Select - You go right ahead and select any pathway for analysis

2. Suggest - The tool can suggest pathways to you according to your pipeline specifications

3. Compare - You can overlay any pathways with each other and do a comparative analysis

You can interactively analyze any renal cancer drug-pathway relationship by using up to four different pathway sources and further refine your analysis with up to 20 different pipeline parameters, including parameters such as presence of mutations, molecular function of targets, stage of development, sub-cellular localization and many more. Each parameter has multi-select options to them and can be used as either an inclusion parameter or exclusion parameter.

User Reports with Graphics:
Each analysis report generated in the Drug Pathway Analyzer includes many different types of graphs and tables which can also be easily downloaded and dropped into applications such as PowerPoint for external presentations outside the tool.

The Pathway Analyzer Comes Integrated with Pipeline Information
With a simple click you can easily and quickly get relevant information about the drug being included in a specific pathway. A typical drug profile reports on, depending on stage of development and available information:

Drug Name & Synonyms
Presentation of drug name and synonyms

Principal Company & Partners
Presentation of principal company and partners

Target and Molecular Function of Target
Described target(s) is/are presented with:
Official Gene Symbol – Chromosome Location – Gene & Protein Name – Molecular Function

Target Localization
Described target(s) is/are presented with primary and alternate localizations.
Target Expression Profiles
Links to protein expression profile(s) of target(s) in various human tissues, cell lines and primary cells, including up to:
48 different normal tissue types
20 different types of cancer
47 cell lines
12 samples of primary blood cells

Mutation
All targets are cross-referenced with the Catalogue of Somatic Mutations in Cancer (COSMIC). It is designed to store and display somatic mutation information and related details and contains information relating to human cancers.

Biological Structures
The identity of available biological structures on drug targets was retrieved from the RCSB Protein Databank for you to easily review what available structures of drug targets exist.

Targeted Pathways
Described target(s) is/are matched for the involvement in cellular pathways according to BioCarta, KEGG, NCI-Nature and NetPath.

Mechanism
Drug mechanism of action

Developmental Projects
Summary field of developmental projects for the drug, including indication, developmental stage and status.
Example:
Cancer, myeloma – Phase II Clinical Trial – Active
Cancer, prostate – Phase III Clinical Trial – Ceased

Drug Description
Short introduction to drug

Compound Data
Compound type, Chemical name, CAS Number and molecular weight

Patent Data
Available patent information related to the drug is presented here.

Fillings and Approvals
Approvals and submissions
Analyst comments

Deals & Licensing
Collaborations and deals
Availability for licensing

Phase IV Data
Available Phase IV development data, developmental history and scientific data.

Phase III Data
Available Phase III development data, developmental history and scientific data.

Phase II Data
Available Phase II development data, developmental history and scientific data.

Phase I Data
Available Phase I development data, developmental history and scientific data.

Phase 0 Data
Available Phase 0 development data, developmental history and scientific data.

Preclinical Data
Available preclinical development data, developmental history and scientific data.

Discovery Data
Available discovery development data, developmental history and scientific data.

System Requirements
- Operating system: Windows (2000/XP/Vista/7/8) and Mac Users are offered Online Access Only
- Browser Application (Internet Explorer)
- Internet access (to access related internet resources)

Download the full report: https://www.reportbuyer.com/product/1816745/

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To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/renal-cancer-drug-pathway-analyzer-2015-300103736.html

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