Blushwood Tree (Hylandia dockrillii)
A Promising Botanical Anticancerous Chemical
Hylandia dockrillii, commonly known as the blushwood tree, is a rainforest tree in the
family Euphorbiaceae endemic to the Atherton Tablelands of Australia.1 It primarily
grows in higher altitudes of 400 to 1100 meters in the warm rain forest and reaches
heights of approximately 25 meters. The tree is not found anywhere else on the
globe. The Atherton Tableland region has a long history of indigenous occupation,
and the Aboriginal people have used the fruit in their traditional medicine. Scientists
learned that the unpalatable seeds contain in the fruit exhibit an inflammatory agent
that causes animal tongues to swell. They isolated the active ingredient in the seeds, a
diterpene ester, which belongs to a new class of chemicals. They named the chemical
of the seed extract tigilanol tiglate or EBC-46. Remarkably, it has now been
demonstrated to be highly anticancerous. 2
Administration and Current Usage
To obtain the active chemicals the seeds must go through an extracting procedure,
after which it then made into liquid, solid capsules, or powder. Most oral forms
involve swallowing the liquid extract or capsules twice to three times daily. For some
skin conditions, it is applied topically. Within clinical settings, EBC-46 is often
administered by direct injection into the tumor. 13
These results prove yet another reason to protect the lush jungles that are dwindling
due to deforestation, but also to restrict the ability of biotechnology and
pharmaceutical companies from patenting anything that occurs in nature.
Dr. Glen Boyle and his team from QIMR Berghofer Medical Research Institute in
Queensland conducted an eight-year study of the fruit seed extract. They observed
that the extracted drug was effective in tumor reduction within a few hours after its
direct injection in terminally ill animal models such as mice, dogs, cats, and horses.
The subjects were diagnosed by veterinarians and given a poor prognosis, most being
considered candidates for euthanasia prior to participating in the study. 3 Further
animal trials have shown that it has activity against four different types of
tumors including basal cell, melanoma, and squamous cell carcinoma, and nearly 75%
of preclinical trials revealed promising results with very little relapse after 1-year
follow-up period and exhibited no side effects.
EBC-46 is currently being evaluated for safety and efficacy in a clinical Phase-I trial in
patients with cutaneous or subcutaneous solid tumors. Such tumors include
melanoma, head and neck cancer, various skin cancers, and Merkel cell carcinoma. In
this trial, EBC-46 is administered locally by direct injection into tumors. The trial is
being conducted in Australia by clinicians in Sydney, Melbourne, Brisbane, and
Adelaide. According to the QBiotics Group, cancer tumors are destroyed within 4-7
days after receiving an EBC-46 injection. 4
Researchers say that the preparation of the drug is a complex technique and human
trials are currently being performed. EBC-46 cannot be synthesized at a commercial
scale and will therefore be manufactured for clinical use by extraction and purification
from blushwood fruit. Meaning it cannot be duplicated chemically and must be
derived from the source. As a result, blushwood plantations will be required to enable
ongoing drug supply. 5
EBC-46 is currently being used as a veterinary anticancer drug and contains a
concentration of phorbol esters. Phorbol esters have been shown to induce apoptosis
and senescence in several cancer cell models. 6, 7 Its exact anticancerous mechanism is
still uncertain. Studies show that tigilanol tiglate (EBC-46) acts directly by disrupting
the tumor blood vessels, and by tumor direct cell killing through a process called
oncosis. 8 It also induces rapid healing of the tumor site. Non-injected tumors may also
be targeted by indirect systemic anti-tumor responses. 9
It is believed that EBC-46 is a protein kinase C regulator that initiates apoptosis of
tumor cells and causes a local inflammatory reaction that recruits the body's
neutrophils to attack the tumor. Protein kinase C (PKC) is a family of serine-
threonine protein kinases that are involved in signal transduction pathways that
regulate growth factor response, proliferation, and apoptosis. 10, 11, 12
1. Airy Shaw, H.K. (1974) Kew Bulletin 29: 329. Type: Queensland, State Forest Reserve 756, Maple L. A.;
holo: K, iso: QRS.
2. The Renegade Pharmacist (2017). EBC46-The Truth About Australian Miracle Berry Extract that Cures
Cancer. Available from https://www.therenegadepharmacist.com/ebc-46-thetruth-about-the-ausrtalian-
3. Health and Natural World (2017). How Brushwood Berries can Destroy Cancer Cells Almost Instantly.
Available from: http:// www.healthyandnaturalworld.com/blushwood-berries-candestroy-cancer-cells-
almost-instantly/. [Cited on 2017 Aug 17].
4. Human - QBiotics - Details of the trial can be found by accessing the Australian New Zealand Clinical
Trial Registry at www.anzctr.org.au and entering “QBiotics” in the search window.
5. That’s Life Magazine (2017). Promising ‘Cancer Cure’ Berries Taken off Sale for Fear of Toxic Home
Remedy Poisoning. Available from:
6. Xiao, Liqing, M. Cecilia Caino, Vivian A. von Burstin, Jose L. Oliva, and Marcelo G. Kazanietz. "Phorbol
Ester–Induced Apoptosis and Senescence in Cancer Cell Models." Methods in enzymology 446 (2008): 123-139.
7. Chianese, Giuseppina, Hawraz Ibrahim M. Amin, Chiara Maioli, Paul Reddell, Peter Parsons, Jason Cullen,
Jenny Johns et al. "Cryptic Epoxytiglianes from the Kernels of the Blushwood Tree (Fontainea
picrosperma)." Journal of natural products 85, no. 8 (2022): 1959-1966.
8. Oncosis can be activated in three different ways: (1) damage to cell membranes, resulting in a loss of
selective permeability, which contributes to the membrane attack complex (MAC) of the complement
pathway; (2) membrane phospholipids degradation via dysregulated phospholipase activity or peroxidation by radical oxygen species (ROS); and (3) disruption of the respiratory chain machinery in mitochondria and a decrease in oxidative phosphorylation and the generation of adenosine triphosphate (ATP). These events
trigger sharp rises in intracellular Ca 2+ concentration, followed by an uncontrolled influx of extracellular water and ions, gradual cell swelling, and rupture.
9. Human - QBiotics
10. Gonzalez-Guerrico, Anatilde M., and Marcelo G. Kazanietz. "Phorbol ester-induced apoptosis in prostate cancer cells via autocrine activation of the extrinsic apoptotic cascade: a key role for protein kinase
Cδ." Journal of Biological Chemistry 280, no. 47 (2005): 38982-38991.
11. Gonzalez-Guerrico, Anatilde M., John Meshki, Liqing Xiao, Fernando Benavides, Claudio J. Conti, and
Marcelo G. Kazanietz. "Molecular mechanisms of protein kinase C-induced apoptosis in prostate cancer cells." BMB Reports 38, no. 6 (2005): 639-645.
12. Yin, Lihong, Nabila Bennani-Baiti, and C. Thomas Powell. "Phorbol ester-induced apoptosis of C4-2 cells requires both a unique and a redundant protein kinase C signaling pathway." Journal of Biological Chemistry 280, no. 7 (2005): 5533-5541.
13. Wender, Paul A., Zachary O. Gentry, David J. Fanelli, Quang H. Luu-Nguyen, Owen D. McAteer, and
Edward Njoo. "Practical synthesis of the therapeutic leads tigilanol tiglate and its analogues." Nature
Chemistry (2022): 1-6.