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Showing posts with label Curcumin. Show all posts
Showing posts with label Curcumin. Show all posts

Friday, 6 December 2019

Impt Tools for Parkinson's: Curcumin Vitamin D and Omega-3

Turmeric contains curcumin, the polyphenol identified as its primary active component and which exhibits over 150 potentially therapeutic activities, which include antioxidant, anti-inflammatory and anti-cancer properties.1

July 08, 2013                   

Turmeric

Story at-a-glance

  • Curcumin crosses the blood-brain barrier and exhibits potent neuroprotective properties, leading researchers to investigate it as a possible drug alternative in the treatment of neurodegenerative disorders such as Parkinson’s disease
  • Unlike Parkinson’s drugs, curcumin, a polyphenol identified as the primary active component of the spice turmeric, it reduces inflammation and oxidative damage in the brain
  • Curcumin has also shown promise for preventing other brain disorders, including dementia, Huntington’s disease and Alzheimer’s disease
  • Parkinson’s disease is related to certain lifestyle factors, including exposure to pesticides, paint and solvents, and vitamin D deficiency; animal-based omega-3 fats are also a powerful defense against Parkinson's

By Dr. Mercola
Most spices have powerful medicinal properties, which is precisely why they've been used to promote healing for thousands of years prior to the advent of modern, synthetic drug-based medicine.  
One such spice is turmeric, the yellow-pigmented "curry spice" often used in Indian cuisine. Turmeric contains curcumin, the polyphenol identified as its primary active component and which exhibits over 150 potentially therapeutic activities, which include antioxidant, anti-inflammatory and anti-cancer properties.1  
Curcumin is capable of crossing the blood-brain barrier, which is one reason why it holds promise as a neuroprotective agent in a wide range of neurological disorders.  
Researchers have investigated curcumin for its potential role in improving Parkinson's disease .

Preliminary results indicate that it may hold even more promise than the drugs currently used for this disorder, many of which (ironically) have serious neurotoxic side effects, including dyskinesia – a movement disorder identical to the symptoms of Parkinson's disease. 


Natural Curcumin Extract Outshines Parkinson's Drugs 

Parkinson's is a neurodegenerative disease caused by a steady depletion of dopamine-producing nerve cells, particularly in the area of your brain referred to as the substantia nigra. Most of the current drug treatments for Parkinson's disease, known as dopamine agonists, focus on replenishing dopamine.  
Although such treatments provide symptomatic relief during early Parkinson's disease, they are ineffective in the long term where they may actually increase symptoms such as tremor, postural instability and cognitive deficits that are common with this disease. They are also associated with motor complications and a laundry list of other strange and disturbing side effects, including: 
EuphoriaNausea
HallucinationsInsomnia
Causing or worsening psychosisUnusual tiredness or weakness
Orthostatic hypotension (a dizzy spell caused by a sudden drop in blood pressure)Dizziness, drowsiness, lightheadedness, or fainting
Increased orgasmic intensityTwitching, twisting, or other unusual body movements
Weight lossPathological addiction (gambling, shopping, internet pornography, hypersexuality)

As researchers noted in the journal Current Pharmaceutical Design:2
"Most of the current pharmacotherapeutic approaches in PD [Parkinson's disease] are aimed at replenishing the striatal dopamine. Although these drugs provide symptomatic relief during early PD, many patients develop motor complications with long-term treatment. Further, PD medications do not effectively tackle tremor, postural instability and cognitive deficits.

Most importantly, most of these drugs do not exhibit neuroprotective effects in patients. Consequently, novel therapies involving natural antioxidants and plant products/molecules with neuroprotective properties are being exploited for adjunctive therapy."
Unlike Parkinson's drugs, curcumin is neuroprotective and several studies strongly support its use for the treatment of Parkinson's. For example:
  • Curcumin showed neuroprotective properties in an animal model of Parkinson's disease; the beneficial effect was thought to be related, in part, to its antioxidant capabilities and its ability to penetrate the brain.3
  • Curcumin alleviated the effects of glutathione depletion, which causes oxidative stress, mitochondria dysfunction and cell death – and is a feature of early Parkinson's disease.4
  • The c-Jun N-terminal kinase (JNK) signaling pathway is involved in dopaminergic neuronal degeneration, which is in turn associated with Parkinson's. Curcumin prevents dopaminergic neuronal death through inhibition of the JNK pathway, and thereby offers a neuroprotective effect that may be beneficial for Parkinson's.5
  • Slow-wriggling alpha-synuclein proteins can cause clumping, which is the first step for diseases such as Parkinson's. Curcumin helps prevent the proteins from clumping.6

 

Curcumin Is a Powerful Ally for Your Brain Health 

For years now turmeric, and its active ingredient curcumin, have shown powerful benefits to your brain health. One of the ways that it works, similar to vitamin D, is modulating large numbers of your genes; in fact, curcumin has been shown to influence more than 700 genes. 
The potential healing power of this spice, which is an important part of Eastern cultural traditions including traditional Chinese medicine and Ayurveda, perhaps first came about when it was noticed that the prevalence of Alzheimer's disease among older adults in India is more than four times lower than the rate in the United States.    
Why such a significant difference?  
Some researchers believe the answer for this drastic disparity in Alzheimer's disease prevalence is a direct result of curcumin. Research has shown that curcumin may help inhibit the accumulation of destructive beta amyloids in the brain of Alzheimer's patients, as well as break up existing plaques. People with Alzheimer's tend to have higher levels of inflammation in their brains, and curcumin is perhaps most known for its potent anti-inflammatory properties. The compound can inhibit both the activity and the inflammatory metabolic byproducts of cyclooxygenase-2 (COX2) and 5-lipooxygenase (5-LOX) enzymes, as well as other enzymes and hormones that modulate inflammation. 
And that's not all. The growing interest in curcumin over the past 50 years is understandable when you consider the many health benefits researchers have found when studying this spice. According to an ever-expanding clinical body of studies, curcumin may help: 
Reduce cholesterol levels Prevent low-density lipoprotein oxidationInhibit platelet aggregation
Suppress thrombosis and myocardial infarctionSuppress symptoms associated with type 2 diabetesSuppress symptoms of rheumatoid arthritis
Suppress symptoms of multiple sclerosis Suppress symptoms of Alzheimer's diseaseInhibit HIV replication
Suppress tumor formationEnhance wound healingProtect against liver damage
Increase bile secretionProtect against cataractsProtect against pulmonary toxicity and fibrosis

 

Two More Important Tools for Parkinson's: Vitamin D and Omega-3 

There is a correlation between insufficient levels of vitamin D and the development of early Parkinson's disease, and research has suggested that long-term deficiency may play a role in the pathogenesis of the disease. There are three major points you want to remember about vitamin D:
  1. Your best source for this vitamin is exposure to the sun, without sunblock on your skin, until your skin turns the lightest shade of pink. While this isn't always possible due to the change of the seasons and your geographic location (and your skin color), this is the ideal to aim for. A safe tanning bed is the next best option, followed by oral vitamin D3 supplementation.
  2. If you do supplement with vitamin D, you'll only want to supplement with natural vitamin D3 (cholecalciferol). Do NOT use the synthetic and highly inferior vitamin D2, which is the one most doctors will give you in a prescription most of the time unless you ask specifically for D3.
  3. Get your vitamin D blood levels checked! The only way to determine the correct dose is to have your blood tested since there are so many variables that influence your vitamin D status. I recommend using Lab Corp in the U.S. Getting the correct test is the first step in this process, as there are TWO vitamin D tests currently being offered: 1,25(OH)D and 25(OH)D.
From my perspective, the preferred test your doctor needs to order is 25(OH)D, also called 25-hydroxyvitamin D, which is the better marker of overall D status. This is the marker that is most strongly associated with overall health. You'll want to optimize your levels according to the chart below. If you currently have Parkinson's disease you will want to keep your vitamin D level in the higher 70-100 ng/ml range to help fight the disease.  
vitamin d levels
  
Animal-based omega-3 fats are also a powerful defense against Parkinson's, as they contain two fatty acids crucial to human health, DHA and EPA. Most of the neurological benefits of omega-3 oils are derived from the DHA component rather than the EPA component. 
In fact, DHA is one of the major building blocks of your brain. About half of your brain and eyes are made up of fat, much of which is DHA -- making it an essential nutrient for optimal brain and eye function. Your brain activity actually depends greatly upon the functions provided by its outer, fatty waxy membrane to act as an electrical nerve-conduction cable. In your brain alone, DHA may help to ward off Parkinson's by:
  • Reducing brain inflammation
  • Stimulating neuron growth, and development and repair of synapses. (Your brain is a vast complex system of nerve cells sending and receiving electrical impulses across junctions called synapses. The small space between the two cells is where the action occurs. One neuron may synapse with as many as 1,000 other neurons.)
  • DHA protects your brain's function by supporting optimal glutamate function. Glutamate and GABA are considered your brain's 'workhorse' neurotransmitters. They work together to control your brain's overall level of excitability, which controls many body processes.
I believe krill oil is your best option for getting animal-based omega-3 fats because of the fact that the omega-3 is attached to phospholipids that dramatically increase its absorption, especially into brain tissue.

Lifestyle Changes to Help Prevent Parkinson's 

Parkinson's disease is related to lifestyle factors, including the following:  
Environmental toxins and pesticidesAspartame consumption
Petroleum-based hydrocarbon solvents, like paint and glueDeficiencies in vitamin D and vitamin B folate
Excess iron in your bodyPasteurized milk

In addition to avoiding these toxic exposures, I recommend lifestyle adjustments including:
  • Exercise regularly, including high-intensity exercise like Peak Fitness. It's one of the best ways to protect against the onset of symptoms of Parkinson's disease
  • Get plenty of sunshine to optimize your vitamin D levels
  • Avoid pesticide and insecticide exposure (as well as exposure to other environmental toxins like solvents)
  • Eat more organic vegetables, which are high in folate, the natural form of folic acid (folate after all comes from foliage)
  • Make sure your body has healthy levels of iron and manganese (neither too much nor too little of either)
  • Consider supplementing coenzyme Q10, which may help to fight the disease. But remember, the oxidized form of coenzyme Q10 called ubiquinone or plain CoQ10 is actually found in elevated levels in neurodegenerative conditions involving enhanced oxidative stress, as it is a residual marker of lipid peroxidation (brain rancidity). This is why ubiquinol, the reduced form that is capable of donating electrons to quench brain-damaging free radicals, while at the same time providing a boost to brain mitochondrial function, is the only logical choice in Parkinson's disease and related neurodegenerative conditions.
As for getting the full benefits that curcumin has to offer, look for a turmeric extract that contains 100 percent certified organic ingredients, with at least 95 percent curcuminoids. The formula should be free of fillers, additives and excipients (a substance added to the supplement as a processing or stability aid), and the manufacturer should use safe production practices at all stages: planting, cultivation, selective harvesting, and then producing and packaging the final product.  
Unfortunately, at the present time there really are no formulations available for the use against cancer. This is because relatively high doses are required and curcumin is not absorbed that well. There is much work being done to provide a bioavailable formulation in the near future. 
In the event you need higher doses (such as in the case of treating cancer), use the curcumin powder and make a microemulsion of it by combining a tablespoon of the powder and mixing it into 1-2 egg yolks and a teaspoon or two of melted coconut oil. Then use a high-speed hand blender to emulsify the powder (be careful when doing so as curcumin is a very potent yellow pigment and can permanently discolor surfaces if you aren't careful).  
Another strategy that can help increase absorption is to put one tablespoon of the curcumin powder into a quart of boiling water. It must be boiling when you add the powder; it will not work as well if you put it in room temperature water and heat the water and curcumin. After boiling it for 10 minutes you will have created a 12 percent solution that you can drink once it has cooled down. It will have a woody taste. The curcumin will gradually fall out of the solution, however. In about six hours it will be a 6 percent solution, so it's best to drink the water within four hours
[-] Sources and References


http://articles.mercola.com/sites/articles/archive/2013/07/08/curcumin-vs-drugs-for-parkinsons.aspx

This article was previously published as:
Curcumin: The Spice That Can Potentially Help Your Health in 150 Different Ways

Wednesday, 27 November 2019

Woman Beats Cancer With Curcumin

Dieneke Ferguson was dying. She was losing her four-year battle with the blood cancer myeloma.
INH Research
Despite three grueling rounds of chemotherapy and four stem cell transplants, the cancer was spreading throughout her body.1
She knew her death would be painful. She faced infections, unstoppable internal bleeding, blood clots, and kidney failure.2
So Ferguson decided to chuck conventional medicine. It hadn’t helped her anyway. She wanted to try a natural cure before it was too late.
She had read on the internet about the cancer-fighting properties of the spice turmeric. She stopped all mainstream medical treatments and began taking 8 grams of curcumin—the active compound in turmeric—each day.
Today, over five years later, she is healthy and leading a normal life. Astounded doctors wrote about her case in the British Medical Journal (BMJ).
Dieneke Ferguson
Dieneke Ferguson, 67, at the Olympics in Brazil.
She felt so good that she traveled from her home in north London to the 2016 Olympics in Brazil, where she carried the Olympic torch.3
Ferguson, 67, says, “I hope my story will lead to more people finding out about the amazing health benefits of curcumin.”4

Doctors: Curcumin Saved Her Life

Her doctors are from Barts Health NHS Trust, the second largest cancer center in London. They wrote in their journal article on Ferguson: “The fact that our patient, who had advanced stage disease and was effectively salvaged while exclusively on curcumin, suggests a potential anti-myeloma effect of curcumin.
“She continues to take daily curcumin and remains in a very satisfactory condition with good quality of life. This case provides further evidence of the potential benefit for curcumin in myeloma.”5

‘A Very Potent Natural Medicine’

Ferguson was diagnosed with myeloma in 2007. In 2011, she stopped her grueling medical regimen and turned to curcumin.
By 2012, tests showed that her cancer was dormant. She no longer had any active cancer-causing cells.
It is estimated that 12,590 Americans (6,660 men and 5,930 women) will die from myeloma this year.6
But researchers say that curcumin might save some of these patients.
Turmeric, the spice from which it is derived, has been used in India as a medicine for thousands of years. It is also a staple of Indian cooking and an ingredient in curry dishes. It is ground from the root of the Curcuma longa plant.7
People in India have far lower rates of cancer compared to Americans. Depending on the type of cancer, the rate can be anywhere from eight to 17 times greater for the U.S. population.
Dr. Ajay Goel is one of the world’s leading researchers in curcumin’s health effects. He is director of the Center for Translational Genomics and Oncology at Baylor University Medical Center.
Dr. Goel has witnessed curcumin’s cancer-fighting power both in the lab and in patients. He states flatly that curcumin has “a very strong anticancer effect.”
While the mechanism behind curcumin’s anticancer effect is not entirely understood, Dr. Goel says it appears curcumin interferes with the ability of cancer cells to divide uncontrollably.

Studies Show Curcumin Stops Many Types of Cancer

Over the past 10 years, studies have found strong evidence that curcumin stops many different types of cancer:
  • A Chinese study at Zhejiang Provincial People’s Hospital in 2012 found that curcumin induces cell death in triple negative breast cancer. This is considered the most aggressive form of breast cancer.
  • UCLA researchers found in 2011 that curcumin activates cancer-fighting enzymes in patients with head and neck cancers.
  • A 2013 study at the University of North Texas Health Science Center found that curcumin suppresses pancreatic cancer tumor growth.
  • A 2006 study published in the journal Neuroscience Letters found that curcumin induces cell death in glioblastoma (brain cancer) cells.8
So why do drug companies and most mainstream doctors ignore curcumin?
It’s because compared to cancer drugs, there is little profit in curcumin supplements. Cancer medications often cost patients hundreds of thousands of dollars a year. Curcumin comes from a natural spice that can’t be patented or sold exclusively. It’s abundant and inexpensive.

Take the Right Kind of Curcumin

Curcumin alone has poor bioavailability. It needs fat to be absorbed by the body.
That’s why Dr. Goel recommends a form called BCM-95. It includes natural oils from the turmeric plant that help your body metabolize curcumin. BCM-95 is widely available at health food stores and online.
Although curcumin is generally safe, you should consult your physician before taking it. People taking blood thinners such as Coumadin (warfarin) should exercise some caution. Curcumin is not a blood thinner itself, but it can increase the effect of Coumadin and similar drugs.
References:
1 http://www.dailymail.co.uk/health/article-5230201/Pensioner-used-turmeric-fight-blood-cancer.html
2 https://www.everydayhealth.com/multiple-myeloma/specialists/how-does-myeloma-cause-death.aspx
3 https://hiddenart.co.uk/details-of-tcurcumin-taken-by-dieneke-ferguson/
4 http://www.dailymail.co.uk/health/article-5230201/Pensioner-used-turmeric-fight-blood-cancer.html
5 http://casereports.bmj.com/content/2017/bcr-2016-218148.full
6 https://www.cancer.net/cancer-types/multiple-myeloma/statistics
7 http://www.dailymail.co.uk/health/article-5230201/Pensioner-used-turmeric-fight-blood-cancer.html
8 https://www.ncbi.nlm.nih.gov/pubmed/16949208

https://www.institutefornaturalhealing.com/2018/01/woman-beats-cancer-with-curcumin/

Turmeric - This Spice Stops Cancer, Study Finds

Prostate cancer is so common in the U.S. that screening is a standard part of men’s checkups. In India, prostate cancer is so rare that it’s not even a concern.
American men get 23 times more prostate cancer than men in India.
by Garry Messick
The story is similar for breast cancer. American women get five times more breast cancer than women in India.[1]
Here’s how the U.S. stacks up to India regarding other cancers:[2]
  • 17 times more lung cancer
  • 14 times more melanoma
  • 12 times more kidney cancer
  • 11 times more colon cancer
  • 9 times more endometrial cancer
  • 8 times more bladder cancer
Scientists believe they’ve discovered India’s anti-cancer secret: turmeric, the yellow powder used in curry dishes.
It is a staple food in the country. People in many parts of India eat it in every meal.
Now, new research shows how turmeric and curcumin, its active ingredient, stop cancer on a molecular level.
The study comes from Japan’s Nara Institute of Science and Technology. The research team looked at a molecule called pentagamavumon-1 (PGV-1). PGV-1 is very similar to a molecule found in curcumin.[3]
The study found that PGV-1 suppresses enzymes that protect cancer cells, causing the cells to die.
The curcumin-derived molecule was effective against a wide range of cancers.
Investigators implanted human cancer cells in mice. When injected with PGV-1, the rodents’ cancer was entirely destroyed.
Professor Jun-ya Kato lead the study. He said that considering the stunning effectiveness and “low amounts of side effects,” PGV-1 should be used to treat cancer.
Previous studies provide strong evidence that curcumin is powerful medicine against cancer:
  • UCLA researchers found in 2011 that curcumin activates cancer-fighting enzymes in patients with head and neck cancers.[4]
  • A 2013 study at the University of North Texas Health Science Center found that curcumin suppresses pancreatic cancer tumors.[5]
  • A 2006 study published in the journal Neuroscience Letters found that curcumin induces cell death in glioblastoma (brain cancer) cells.[6]
  • A Chinese study showed that curcumin makes stomach cancer less resistant to chemotherapy.[7]
  • A study at MD Anderson Cancer Center showed that curcumin slowed the progression of multiple myeloma (blood cancer).[8]
With all this evidence (and this is by no means a complete list) you may be wondering why curcumin isn’t widely prescribed for the prevention and treatment of cancer.

Curcumin: India’s Anti-Cancer Secret

People in India get curcumin by eating turmeric at almost every meal. Most Americans are not willing to do this. That’s why, for most of us, curcumin supplements are the best option for cancer prevention.
Curcumin is safe for just about everyone. However, people taking blood thinners such as Coumadin (warfarin) should consult their doctor. Curcumin can increase the effect of Coumadin and other similar drugs.
Curcumin by itself is not easily absorbed by the body. Fat increases bioavailability. So taking curcumin with a meal that includes fat improves absorption.
In the war on cancer, mainstream medicine’s main weapons are surgery, chemo, and radiation. They often do more harm than good.
India clearly has a better answer…a safe, natural way to stop one of our deadliest health problems.
Editor’s Note: If you’re worried about cancer, you need to read our monthly journal, Independent Healing. It’s your best source for unbiased, evidence-based medical advice. Discover The Cancer Kill Code. It’s a secret natural trigger that detonates cancer’s self-destruct button.
Find out more HERE.
Related Articles
[1]http://www.greenmedinfo.com/article/curcumin-induces-apoptosis-triple-negative-breast-cancer-cells
[2]https://nutritionfacts.org/2015/05/05/why-are-cancer-rates-so-low-in-india/
[3]https://www.nature.com/articles/s41598-019-51244-3
[4]https://www.theatlantic.com/health/archive/2011/09/turmeric-the-potential-cure-for-cancer-found-in-indian-food/245115/
[5]http://www.greenmedinfo.com/article/efficacy-liposomal-curcumin-human-pancreatic-tumor-xenograft-model-inhibition
[6]http://www.greenmedinfo.com/article/efficacy-liposomal-curcumin-human-pancreatic-tumor-xenograft-model-inhibition
[7]http://beatcancer.org/blog-posts/curcumin-and-cancer-part-two

[8]http://beatcancer.org/blog-posts/curcumin-and-cancer-part-two
https://www.institutefornaturalhealing.com/2019/11/this-spice-stops-cancer-study-finds/

Wednesday, 13 November 2019

Cancer as a Curable Metabolic Disease

We have lost the war against cancer.  This becomes obvious by taking a quick look at the chart below.  Cancer Death Rates have declined slightly since 1975 due to reduction in lung cancer rates from decreased cigarette consumption.  Otherwise, there has been little change. 

Cancer as a Metabolic Disease
Published on jeffreydachmd.com

Lung cancer cell division, SEM
Above left lung cancer cell dividing courtesy of NIH.  Below chart image courtesy 
The Failure of Chemotherapy
In 1997, John C. Bailar M.D. explained how we lost the "War Against Cancer": 
"The failure of chemotherapy to control cancer has become apparent even to the oncology establishment."  
Here is a quote from Dr. Haines in Lancet:  
"The misplaced battlefield analogy has led to 40 years of toxic and overly aggressive chemotherapy in incurable solid cancers for which no studies have shown that maximum tolerated doses of chemotherapy achieve longer survival or better quality of life than do minimum effective doses. This approach has led to inappropriate and toxic therapies for many patients ... "
Dr Carlos Garcia says cancer treatment with chemotherapy has a 97% failure rate: Three Per Cent Efficacy Of CHEMO On Cancer by Carlos Garcia MD.

Chemotherapy Kills Normal Cells As Well As Cancer Cells
chemotherapy drug
The obvious flaw in cancer chemotherapy treatment is the non-specificity.  In other words, cancer chemotherapy kills cancer cells as well as normal cells.  This unwanted toxicity to normal cells accounts for the adverse side effects of chemotherapy, namely nausea, vomiting, loss of appetite, weight loss, bone marrow suppression with anemia, hair loss etc.
Finding a Selective Cancer Treatment, Leaving Normal Cells Unharmed
Cancer As Metabolic Disease Seyfried
Image above, cover of the book "Cancer as a Metabolic Disease" by Dr Thomas Seyfried courtesy of the Examiner
The optimal cancer treatment is one that kills cancer cells while leaving normal cells unharmed.  Dr Seyfried's article, "Cancer as a Metabolic Disease," points the way to this goal.(1)  Dr. Seyfried says: "cancer is primarily a metabolic disease involving disturbances in energy production through respiration and fermentation."(1)  Electron microscope studies have shown abnormalities in the mitochondria of cancer cells.(2)  The cancer cell's mitochondria have undergone "metabolic reprogramming," thereby providing a key which can be exploited to devise a more selective cancer treatment.(3,4) 

Drs Ko and Pederson, 3BP and Hexokinase II

Basic science studies by Drs Ko and Pedeson have uncovered the exact details of the metabolic reprogramming of the mitochondria of cancer cells.  In cancer cells, an embryonic form of Hexokinase called Hexokinase II has been attached to the membrane pores of the mitochondria (called VDAC voltage dependent anion channels).  Hexokinase II is the first enzyme in glucose utilization and its location on the outer membrane pores allows for the massive utilization of glucose to feed the rapidly growing tumor mass.  Separation of the Hexokinase II from the VDAC pore on the outer mitochondrial membrane triggers apoptosis (programmed cell death) of the cancer cell while sparing normal cells.(5,6)
Dr_Ko_Dr_Pedersen_Drs_Khan
Above image: Dr. Young Ko and Dr. Peter Pedersen with Dr. Humaira Khan, Medicor CEO (left) and Dr. Akbar Khan Medicor Medical Director (right) at the Medicor Office in Toronto, December 2008. Courtesy of Medicor.

Discovery of 3BP by Dr. Ko

Drs Ko and Pederson discovered a small molecule called 3BP which throws a "monkey wrench" into the metabolic machinery of the cancer cell, and induces apoptosis via separation of Hexokinase II from the outer mitochondrial membrane.(7)(27, 28)
3BP (3 Bromo Pyruvate) is a small non-toxic molecule that induces apoptosis in cancer cells while sparing normal cells, thus providing the most promising cancer treatment we have seen in many years.  In-fighting over patent rights by the key players has delayed drug development and commercialization.  Unfortunately, 3BP as a cancer treatment may never come to fruition.(7)

Natural Compounds That Disassociate Hexokinase II From VDAC

Human_VDAC
Image Above VDAC courtesy of NIH.
Thankfully, there are many other compounds in the natural world that act on this same mechanism of selectively inducing apoptosis in cancer cells while sparing normal cells.   Many of these have already been commercialized and are available at the health food store.

Resveratrol and Pterostilbenes

Resveratrol from grapes and its derivative Pterostilbene have been extensively studied and demonstrate striking anticancer activity.  Studies show that Pterostilbene induces apoptosis via the mitochondrial pathway in breast cancer cell lines. See the article by Moon and another article by Pei-Ching Hsiao.  His study used acute myeloid leukemia cells, finding pterostilbene induced apoptosis in cancer cells via mitochondrial pathways (with activation of caspase system).  Another study by Alosi on Pterostilbene in Breast Cancer also showed similar findings with apoptosis induced by mitochondrial pathways.  Another more recent study by Wang in 2012 showed Pterostilbene induces apoptosis and cell cycle arrest in breast cancer cells.  See my previous article on this.
Mitochondria
Abov image : electron microscope image of normal mitochondria courtesy of NIH.

Methyl Jasmonate

Methyl Jasmonate has been studied and found to disassociate Hexokinase II from the outer mitochondria membrane (at the VDAC) thus inducing apoptosis in cancer cells.  Methyl jasmonate is ubiquitous in the plant world and found in the jasmine flower.  It is used extensively by the fragrance industry for perfumes, and is available as one of many Jasmine teas.(8,9,10)

Oroxylin A – Chinese Skullcap

Oroxylin A is found in Chinese skullcap a medicinal plant, Scutellaria baicalensis Georgi.  Researchers found Oroxylin A inhibits glycolysis and the binding of hexokinase II (HK II) with mitochondria in human breast carcinoma cell lines, thus inducing apoptosis (11,12)

Curcumin

Curcumin was studied by Dr Wang in an animal model of colorectal cancer showing Curcumin inhibits aerobic glycolysis and induces mitochondrial-mediated apoptosis through hexokinase II in human colorectal cancer cells in vitro.(13)(31)  Curcumin is available at the health food store.

Betulinic Acid

Betulinic acid naturally occurs in the bark of white birch trees and triggers mitochondrial apoptosis in cancer cells while sparing normal cells (14)  Dr, Simone Fulda from Ulm Germany has written a number of important papers on targeting mitochondria in cancer cells with various drugs and natural compounds.(14,15)

Berberine – Oregon Grape

Oregon_Grape_Berberine_Jeffrey_Dach_MD
 Image Above Oregon Grape courtesy of wikimedia commons.(31,32)
Berberine derived from the Oregon Grape plant is widely available as a botanical supplement at the health food store for blood sugar control.  Berberine also shows striking anti-cancer activity, inducing apoptosis via mitochondrial pathways in numerous studies.  See this 2014 review in Molecules,  Berberine as an "Epiphany Against Cancer".(32)

Artemesinin (Chinese Wormwood)

An anti-malarial Chinese herb, artemesia, has been found to have profound anti-cancer activity against multiple cancer cell lines. Studies show induction of apoptosis through mitochondrial pathways. Approximately 400 studies have been published in the scientific literature in recent years.
Click on this LINK for the list of publications. Click on this LINK for an excellent review.

Vitamin K

Vitamin K has been available for many years with heath benefits in blood coagulation, bone density, and prevention of soft tissue calcification.  See my previous article on Vitamin K.  Another surprising benefit of Vitamin K is cancer prevention.  A number of cell culture and animal xenograft studies shows that vitamin K2 induces apoptosis, programmed cell death, in cancer cells.(18-26)  There were a number of different cancers studied including Glioblastoma, Hepatocellular Cancer, Lung Cancer, Prostate Cancer, etc.(18-26)  Based on these reports, one might suggest adding Vitamin K  to a supplement program for anyone seeking to prevent cancer, or cancer recurrence after treatment.
Articles with related interest:

Addendum:

Selectively Killing Cancer Cells Leaving Normal Cells Unharmed – Apoptosis Through Mitochondrial Pathways
Mebendazole – Re purposing Old Drugs as Anti-Cancer Agents:
Researchers screened 2000 drugs currently approved for human use for anti-cancer activity against virulent melanoma cancer cell lines. They discovered mebenzadole as the most promising agent.  
"Mebendazole treatment induces apoptosis through the intrinsic and extrinsic (mitochondrial) pathways in melanoma cells but not in melanocytes ... After treatment with 0.5 μmol/L mebendazole for 14 h, we observed overall microtubular network disarray in melan-a, M-14, and SK-Mel-19 cells, characterized by diffuse staining."(33-37)

Links and References:

1) https://www.ncbi.nlm.nih.gov/pubmed/24343361
Carcinogenesis. 2014 Mar;35(3):515-27.
Cancer as a metabolic disease: implications for novel therapeutics.
Seyfried TN1, Flores RE, Poff AM, D'Agostino DP.
1Biology Department, Boston College, Chestnut Hill, MA 02467, USA and.
Emerging evidence indicates that cancer is primarily a metabolic disease involving disturbances in energy production through respiration and fermentation. The genomic instability observed in tumor cells and all other recognized hallmarks of cancer are considered downstream epiphenomena of the initial disturbance of cellular energy metabolism. The disturbances in tumor cell energy metabolism can be linked toabnormalities in the structure and function of the mitochondria.
Cancer growth and progression can be managed following a whole body transition from fermentable metabolites, primarily glucose and glutamine, to respiratory metabolites, primarily ketone bodies.
2) https://www.ncbi.nlm.nih.gov/pubmed/19703662
Int J Biochem Cell Biol. 2009 Oct;41(10):2062-8.
Electron microscopy morphology of the mitochondrial network in human cancer.
Arismendi-Morillo G.
Mitochondria have been implicated in the process of carcinogenesis, which includes alterations of cellular metabolism and cell death pathways. The aim of this review is to describe and analyze the electron microscopy morphology of the mitochondrial network in human cancer. The structural mitochondrial alterations in human tumors are heterogeneous and not specific for any neoplasm. These findings could be representing an altered structural and functional mitochondrial network. The mitochondria in cancer cells, independently of histogenesis, predominantly are seen with lucent-swelling matrix associated with disarrangement and distortion of cristae and partial or total cristolysis and with condensed configuration in minor scale. Mitochondrial changes are associated with mitochondrial-DNA mutations, tumoral microenvironment conditions and mitochondrial fusion-fission disequilibrium.
Functionally, the structural alterations suppose the presence of hypoxia-tolerant and hypoxia-sensitive cancer cells. Possibly, hypoxia-tolerant cells are related with mitochondrial condensed appearance and are competent to produce adequate amount of ATP by mitochondrial respiration. Hypoxia-sensitive cells are linked with lucent-swelling and cristolysis mitochondria profile and have an inefficient or null oxidative phosphorylation, which consequently use the glycolytic pathway to generate energy.Additionally, mitochondrial fragmentation is associated with apoptosis; however,alterations in the mitochondrial network are linked with the reduction in sensitivity to apoptosis induces and/or pro-apoptotic conditions. Pharmacological approaches designed to act on both glycolysis and oxidative phosphorylation can be considered as a new approach to selectively kill cancer cells.
3) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311998/
Cancer Cell. Mar 20, 2012; 21(3): 297–308.
Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate
Patrick S. Ward1,2 and Craig B. Thompson1,*
4) Tumor_Cell_Metabolism_Cancers_Achilles_Heel_Kroemer_2008 
Cancer Cell  Volume 13, Issue 6, 10 June 2008, Pages 472–482
Tumor Cell Metabolism: Cancer's Achilles' Heel by  Guido Kroemer
Jacques Pouyssegur
Ko and Pederson
5) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714668/
Semin Cancer Biol. Feb 2009; 19(1): 17–24.
Hexokinase-2 bound to mitochondria: Cancer's stygian link to the "Warburg effect" and a pivotal target for effective therapy[star]
Saroj P. Mathupala, Young H. Ko, and Peter L. Pedersen
6) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890051/
Biochim Biophys Acta. 2010 Jun–Jul; 1797(6-7): 1225–1230.
The Pivotal Roles of Mitochondria in Cancer: Warburg and Beyond and Encouraging Prospects for Effective Therapies
Saroj P. Mathupala,1 Young H. Ko,3 and Peter L. Pedersen*,2
7) https://www.thefreelibrary.com/War+on+cancer%3A+3BP+and+the+metabolic+approach+to+cancer%3A+a+visit+with...-a0332893717
Townsend Letter › June 1, 2013
War on cancer: 3BP and the metabolic approach to cancer: a visit with Peter Pedersen and Young Hee Ko
Methyl Jasmonate
8) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933403/
Int J Cell Biol. 2014; 2014: 572097.
Methyl Jasmonate: Putative Mechanisms of Action on Cancer Cells Cycle, Metabolism, and Apoptosis
Italo Mario Cesari,* Erika Carvalho, Mariana Figueiredo Rodrigues, Bruna dos Santos Mendonça, Nivea Dias Amôedo, and Franklin David Rumjanek
Laboratório de Bioquímica e Biologia Molecular do Câncer, Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Avenida Carlos Chagas Filho 373, Prédio CCS, Bloco E, Sala 22, Ilha do Fundão, Cidade Universitária, 21941-902 Rio de Janeiro, RJ, Brazil
Br J Pharmacol. 2014 Feb;171(3):618-35. doi: 10.1111/bph.12501.
Methyl jasmonate sensitizes human bladder cancer cells to gambogic acid-induced apoptosis through down-regulation of EZH2 expression by miR-101.  Wang Y1, Xiang W, Wang M, Huang T, Xiao X, Wang L, Tao D, Dong L, Zeng F, Jiang G.
Gambogic acid (GA) and methyl jasmonate (MJ) are increasingly being recognized as novel natural anticancer compounds. Here, we investigated the antitumour effects of GA in combination with MJ on human bladder cancer cells.
EXPERIMENTAL APPROACH:Cell viability was detected by cell counting kit-8 assay. Cell apoptosis was assessed by Hoechst 33258 staining and flow cytometry. Protein levels were determined by immunoblotting and expressions of mRNA and miRNAs by RT-PCR. Differential expressions of a group of downstream genes were identified using microarray analysis.
KEY RESULTS:MJ significantly sensitized bladder cancer cells to GA-induced growth inhibition and apoptosis while sparing normal fibroblasts. MJ enhanced GA-induced activation of caspase-3 and caspase-9, and down-regulated the expression of XIAP. Furthermore, treatment of bladder cancer cells with a combination of GA and MJ induced synergistic inhibition of the enhancer of zeste homologue 2 (EZH2) expression, whereas miR-101 expression was up-regulated. Conversely, knockdown of miR-101 restored this decreased expression of EZH2 and suppressed the inhibitory effect of GA and MJ on the growth of bladder cancer cells. Microarray analysis showed that genes closely associated with bladder cancer development were significantly down-regulated by GA and MJ. In a s.c. xenograft mouse model of human bladder carcinoma, the combination of GA and MJ exerted an increased antitumour effect compared with GA alone.
CONCLUSION AND IMPLICATIONS:MJ sensitizes bladder cancer cells to GA-inducedapoptosis by down-regulating the expression of EZH2 induced by miR-101. Thus, the combination of selective anti-cancer agents MJ and GA could provide a novel strategy for treating human bladder cancer.
10) https://www.phytotechlab.com/detail.aspx?ID=1176
METHYL JASMONATE Product ID: J389 Storage Temperature: 2 to 6°C
CAS Number: 39924-52-2
Description:  >95% Purity
Methyl Jasmonate (MeJA) is a key signaling hormone associated with necrotropic/herbivore stress which affects plant defense responses as well as growth and development
MeJA, 2-Pentenylcyclopentanone-3-acetic acid, Methyl 3-oxo-2-(pent-2-enyl)cyclopentaneacetate
Form: Liquid
Formula: C13H20O3
FW: 224.3
Solubility: Miscible with EtOH
Plant Tissue Culture Tested
Tariff Code: 2918.30.9000
BEFORE ORDERING PLEASE NOTE:
THIS PRODUCT, LIKE ALL PRODUCTS FROM PHYTOTECH LABS, IS FOR RESEARCH USE ONLY. WE CANNOT SELL TO CUSTOMERS WHO INTEND TO USE METHYL JASMONATE FOR HUMAN USE.
This product cannot be shipped to residential addresses; only shipments to bona fide research institutions and companies will be accepted.

Oroxylin A
11) https://www.nature.com/cddis/journal/v4/n4/full/cddis2013131a.html
Cell Death and Disease (2013) 4, e601
Oroxylin A induces dissociation of hexokinase II from the mitochondria and inhibits glycolysis by SIRT3-mediated deacetylation of cyclophilin D in breast carcinoma by L Wei1,2, Y Zhou1,2, Q Dai1, C Qiao1, L Zhao1, H Hui1, N Lu1 and Q-L Guo1
1State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Department of Physiology, China Pharmaceutical University, Nanjing, The People's Republic of China
Correspondence: Q-L Guo or N Lu, State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Department of Physiology, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, The People's Republic of China.
Oroxylin A is a major active component of the Chinese traditional medicinal plant Scutellaria baicalensis Georgi, which has been reported as a potential anticancer drug. We demonstrated that, Oroxylin A inhibited the glycolysis and the binding of hexokinase II (HK II) with mitochondria in human breast carcinoma cell lines, which was dependent on sirtuin-3 (SIRT3). The level of SIRT3 in mitochondria was increased by Oroxylin A. Then SIRT3 deacetylated cyclophilin D, diminished its peptidyl-prolyl cis-trans isomerase activity and induced its dissociation from the adenine nucleotide translocator. Finally, SIRT3-induced inactivation of cyclophilin D resulted in the detachment of mitochondrial HK II and the inhibition of glycolysis. These results have important implications for the metabolism reprogramming effect and the susceptibility to Oroxylin A-induced mitochondrial cytotoxicity through the regulation of SIRT3 in breast carcinoma.
Qiao, Chen, et al. "UCP2‐related mitochondrial pathway participates in oroxylin A‐induced apoptosis in human colon cancer cells." Journal of cellular physiology (2014).
Oroxylin A is a flavonoid extracted from the root of Scutellaria baicalensis Georgi. Our previous research demonstrated that oroxylin A have various anti-tumor effects including apoptosis, cell cycle arrest, drug-resistant reversion and others. This paper explores the mechanism how oroxylin A induce apoptosis by regulating uncoupling protein 2 (UCP2) in human colon cancer cells.
We found that the inhibition of UCP2 by UCP2 siRNA significantly increased the sensitivity of cells to drugs, reactive oxygen species (ROS) generation and the opening of mitochondrial permeability transition pore (MPTP) of CaCo-2 cells. We also found that UCP2 inhibition could lead to ROS-mediated MPTP activation. Furthermore, we demonstrated that oroxylin A triggered MPTP-dependent pro-apoptotic protein release from mitochondria to matrix and then induced apoptotic cascade by inhibiting UCP2. Intriguingly, the inhibition of UCP2 by oroxylin A was able to block Bcl-2 translocation to the mitochondria, keeping MPTP at open-state. In conclusion, we have demonstrate that UCP2 play a key role in mitochondrial apoptotic pathway; UCP2's inhibition by oroxylin A triggers the MPTP opening, and promotes the apoptosis in CaCo-2 cells.
Curcumin
13) https://www.ncbi.nlm.nih.gov/pubmed/25229889
Anticancer Drugs. 2014 Sep 16. [Epub ahead of print]
Curcumin inhibits aerobic glycolysis and induces mitochondrial-mediated apoptosis through hexokinase II in human colorectal cancer cells in vitro.
Wang K1, Fan H, Chen Q, Ma G, Zhu M, Zhang X, Zhang Y, Yu J.
1aJiangsu Institute of Cancer Research bJiangsu Research Institute of Geriatrics, Nanjing, China.
Curcumin, the major pigment of the dietary spice turmeric, has the potential for chemoprevention by promotion of apoptosis. Here, we investigated the molecular mechanisms of curcumin in glycolytic inhibition and apoptotic induction in human colorectal cancer HCT116 and HT29 cells. On the one hand, curcumin downregulated the expression and activity of hexokinase II (HKII) in HCT116 and HT29 cells in a concentration-dependent manner, but had little effect on the other key glycolytic enzymes (PFK, PGM, and LDH).
On the other, curcumin induced dissociation of HKII from the mitochondria, resulting in mitochondrial-mediated apoptosis. Furthermore, the phosphorylation of mitochondrial HKII through AKT was responsible for the curcumin-induced dissociation of HKII, which was different from the mechanism of HKII inhibitor 3-BrPA. These results have important implications for the metabolism reprogramming effect and the susceptibility to curcumin-induced mitochondrial cytotoxicity through the regulation of HKII, and provide a molecular basis for the development of naturally compounds as novel anticancer agents for colorectal carcinoma.
14) https://www.ncbi.nlm.nih.gov/pubmed/20486070
Planta Med. 2010 Aug;76(11):1075-9.
Modulation of apoptosis by natural products for cancer therapy.
Fulda S1. Children's Hospital, Ulm University, Ulm, Germany.
Fulda, Simone, Lorenzo Galluzzi, and Guido Kroemer. "Targeting mitochondria for cancer therapy." Nature reviews Drug discovery 9.6 (2010): 447-464.
Mitochondria are the cells' powerhouse, but also their suicidal weapon store.
Dozens of lethal signal transduction pathways converge on mitochondria to cause the permeabilization of the mitochondrial outer membrane, leading to the cytosolic release of pro-apoptotic proteins and to the impairment of the bioenergetic functions of mitochondria.
The mitochondrial metabolism of cancer cells is deregulated owing to the use of  glycolytic  intermediates, which are normally destined for oxidative phosphorylation, in anabolic reactions. Activation of the cell death machinery in cancer cells by inhibiting tumour-specific alterations of the mitochondrial metabolism or by stimulating mitochondrial membrane permeabilization could therefore be promising therapeutic approaches.
16) Mitochondrial_inhibitors_cancer_therapy_Pharmaceutical_Ramsay_2011 Ramsay, Emma E., Philip J. Hogg, and Pierre J. Dilda. "Mitochondrial metabolism inhibitors for cancer therapy." Pharmaceutical research 28.11 (2011): 2731-2744.
17) Mitochondrial_permeability_target_anticancer_Dalla_2014  Dalla Via, Lisa, et al. "Mitochondrial permeability transition as target of anticancer drugs." Current pharmaceutical design 20.2 (2014): 223-244.

Cancer. 2006 Feb 15;106(4):867-72.
The effect of menatetrenone, a vitamin K2 analog, on disease recurrence and survival in patients with hepatocellular carcinoma after curative treatment: a pilot study. Mizuta T1, Ozaki I, Eguchi Y, Yasutake T, Kawazoe S, Fujimoto K, Yamamoto K. 1Department of Internal Medicine, Saga Medical School, Japan.
19) https://www.ncbi.nlm.nih.gov/pubmed/23505456
PLoS One. 2013;8(3)  Postoperative use of the chemopreventive vitamin K2 analog in patients with hepatocellular carcinoma. Zhong JH1, Mo XS, Xiang BD, Yuan WP, Jiang JF, Xie GS, Li LQ. 1Hepatobiliary Surgery Department, Tumor Hospital of Guangxi Medical University, Nanning, People's Republic of China.
20) https://www.ncbi.nlm.nih.gov/pubmed/16010434
Int J Oncol. 2005 Aug;27(2):505-11.
Vitamins K2, K3 and K5 exert in vivo antitumor effects on hepatocellular carcinoma by regulating the expression of G1 phase-related cell cycle molecules.
Kuriyama S1, Hitomi M, Yoshiji H, Nonomura T, Tsujimoto T, Mitoro A, Akahane
21) https://www.ncbi.nlm.nih.gov/pubmed/15508263
Acta Neurol Belg. 2004 Sep;104(3):106-10.
Comparison of vitamins K1, K2 and K3 effects on growth of rat glioma and human glioblastoma multiforme cells in vitro. Oztopçu P1, Kabadere S, Mercangoz A, Uyar R. 1Osmangazi University Art and Sciences Faculty Department of Biology, Eskişehir, Türkiye.
22) https://www.ncbi.nlm.nih.gov/pubmed/19424596
Int J Mol Med. 2009 Jun;23(6):709-16.
Growth inhibitory effects of vitamin K2 on colon cancer cell lines via different types of cell death including autophagy and apoptosis.  Kawakita H1, Tsuchida A, Miyazawa K, Naito M, Shigoka M, Kyo B, Enomoto M, Wada T, Katsumata K, Ohyashiki K, Itoh M, Tomoda A, Aoki T.  1Third Department of Surgery, Tokyo Medical University, Tokyo, Japan.
23) https://www.ncbi.nlm.nih.gov/pubmed/12888897
Int J Oncol. 2003 Sep;23(3):627-32.
Apoptosis induction of vitamin K2 in lung carcinoma cell lines: the possibility of vitamin K2 therapy for lung cancer.  Yoshida T1, Miyazawa K, Kasuga I, Yokoyama T, Minemura K, Ustumi K, Aoshima M, Ohyashiki K.      1First Department of Internal Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan.
24) https://www.ncbi.nlm.nih.gov/pubmed/19929921
J Gastroenterol Hepatol. 2010 Apr;25(4):738-44. doi: 10.1111/j.1440-1746.2009.06085.x. Epub 2009 Nov 19. Naturally occurring K vitamins inhibit pancreatic cancer cell survival through a caspase-dependent pathway. Showalter SL1, Wang Z, Costantino CL, Witkiewicz AK, Yeo CJ, Brody JR, Carr BI.     1Department of Surgery, Jefferson Center for Pancreatic, Biliary and Related Cancers, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
25) https://www.ncbi.nlm.nih.gov/pubmed/17611688
Int J Oncol. 2007 Aug;31(2):323-31.
Vitamins K2, K3 and K5 exert antitumor effects on established colorectal cancer in mice by inducing apoptotic death of tumor cells.  Ogawa M1, Nakai S, Deguchi A, Nonomura T, Masaki T, Uchida N, Yoshiji H, Kuriyama S.
26) https://www.ncbi.nlm.nih.gov/pubmed/23875252
Pharmazie. 2013 Jun;68(6):442-8.
Vitamin K4 induces tumor cytotoxicity in human prostate carcinoma PC-3 cells via the mitochondria-related apoptotic pathway.
Jiang Y1, Yang J, Yang C, Meng F, Zhou Y, Yu B, Khan M, Yang H.
1School of Life Sciences, Liaoning Provincial Key Laboratory of Biotechnology and Drug Discovery, Liaoning Normal University, Dalian, PR China.
Xian, Shu-Lin, et al. "." Asian Pacific journal of cancer prevention: APJCP 15.7 (2014): 3175.

28) Chen, Zhao, et al. "Role of mitochondria-associated hexokinase II in cancer cell death induced by 3-bromopyruvate." Biochimica et Biophysica Acta (BBA)-Bioenergetics 1787.5 (2009): 553-560.

United States Patent 6469061
Inventors: Flescher, Eliezer (Hod Hasharon, IL), Fingrut, Orit (Kfar-Sava, IL)
Application Number: 09/825347
Publication Date: 10/22/2002
Filing Date: 04/04/2001

30) Methyl Jasmonate: A New Treatment for B-CLL?.
Alain Berrebi, MD1, Lucette Bassous1,*, Rinat Borenshtain, PhD2,* and Eliezer Flescher, PhD3,*  1 Hematology, Kaplan Medical Center, Rehovot, Israel; 2 Sepal Pharma, Nes Ziona, Israel and 3 Immunology, Tel Aviv University, Tel Aviv, Israel.

CEO Dr. Frederic Revah, PhD
Sepal Pharma, Nes Ziona
Registered Office P.O.Box: 333
Ness Ziona, 74103  Israel
Tel. 08-9302088
Web Site https://www.sepalpharma.com

Aggarwal, Bharat, et al. "Prevention and treatment of colorectal cancer by natural agents from Mother Nature." Current colorectal cancer reports 9.1 (2013): 37-56.

Guamán Ortiz, Luis Miguel, et al. "Berberine, an Epiphany Against Cancer." Molecules19.8 (2014): 12349-12367.

Anti-Parasitic Drug Vermox  (mebendazole)

Nygren, Peter, and Rolf Larsson. "Drug repositioning from bench to bedside: Tumour remission by the antihelmintic drug mebendazole in refractory metastatic colon cancer." Acta Oncologica 53.3 (2014): 427-428.

34) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096024/
Pantziarka, Pan et al. "Repurposing Drugs in Oncology (ReDO)—mebendazole as an Anti-Cancer Agent." ecancermedicalscience 8 (2014): 443. PMC. Web. 13 Jan. 2015.

Doudican, Nicole, et al. "Mebendazole induces apoptosis via Bcl-2 inactivation in chemoresistant melanoma cells." Molecular Cancer Research 6.8 (2008): 1308-1315.

36)  https://neuro-oncology.oxfordjournals.org/content/early/2011/07/14/neuonc.nor077.full  Bai, Ren-Yuan, et al. "Antiparasitic mebendazole shows survival benefit in 2 preclinical models of glioblastoma multiforme." Neuro-oncology (2011): nor077.

37) Mebendazole metastatic adrenocortical carcinoma Dobrosotskaya Endocrine practice 2011 Dobrosotskaya, I. Y., et al. "Mebendazole monotherapy and long-term disease control in metastatic adrenocortical carcinoma." Endocrine practice: official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists 17.3 (2011): e59.
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