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Full-Text Excerpt of The Eggplant Cancer Cure - Chapter 4

A Treatment for Skin Cancer and New Hope for Other Cancers From Natures Pharmacy

by Dr. Bill E. Cham, Ph.D.
$24.95 - 132 pages, hardcover


From the Past to a New Era



Fig 4-1

Fig. 4-1: Eggplant produces glycoalkaloids which are extracted and purified then incorporated into the cream, Curaderm BEC5, which is applied to a skin cancer resulting in the complete removal of all cancer cells without affecting normal cells and healing of the treated lesion with exceptional cosmetic results.


Research is the first step in biopharmaceutical product development. Initially this involves optimization of chemical structures into leading compounds. Once a leading compound has been identified, the pre-clinical phase commences.

BEC - Solasodine Glycosides

Our research has resulted in the identification and characterization of a mixture of solasodine glycosides consisting mainly of solasonine and solamargine from various plant sources including edible fruit such as the eggplant. The actives were termed BEC which is a standardized mixture of the two triglycosides, solasonine, solamargine and their corresponding di-and monoglycosides 5-15.

Fig 4-2

Fig. 4-2: BEC is a standardized mixture of sugar-bound Solasodine. The two main glycoalkaloids are Solasonine and Solamargine. All of the glycoalkaloids are made up of the steroid (aglycone meaning without sugar) Solasodine and one or more of the sugars rhamnose, glucose or galactose.

Pre-Clinical Phase

In the pre-clinical phase, we evaluated BEC for possible therapeutic potential by conducting Ex vivo and In vivo studies.

Ex Vivo studies have demonstrated that BEC was effective against a wide spectrum of human cancers and that BEC was selectively killing cancer cells without harming normal cells 16-27.

Fig 4-3

Fig. 4-3: Effect of BEC on various primary cell lines and cell cultures. This figure shows that at a concentration of 6 ug/ml of BEC, all Ovarian cancer cells are killed but no Bone Marrow cells are effected.

In Vivo studies of BEC with terminal tumours in mice, rats and large animals (horses) clearly established that BEC cured terminal tumours in animals.

The safety of BEC administration was also shown 15, 19, 28-36.

Fig 4-4

Fig. 4-4: This shows that two doses of BEC cured 42% whereas three and four doses cured 92% of the mice that originally had terminal cancer. All untreated mice with the cancer died at day 20.

Phase I Clinical Trials

Here we have to distinguish between the topical application (cream) as opposed to internal use such as oral or intravenous administration. Phase I clinical trials tested BEC for safety (adverse effects) dosage tolerance, metabolism, excretion and pharmacodynamics in a small group of subjects.

BEC, at various concentrations up to 50% in a cream formulation, was shown to be very safe 15, 17-20, 37-43. BEC when used as Curaderm BEC5 for treating non melanoma skin cancers could not be detected in the blood when analyzed for, by a very sensitive procedure, using GCMS.

So, when Curaderm BEC5 is used, no systemic absorption occurs, this is not surprising since Curaderm BEC5 contains much less BEC than is found in the eggplant. Hence, Curaderm BEC5 is extremely safe regarding BEC content! BEC when used in our studies in cream formulations established that these preparations were well tolerated and safe. Analyses of blood and urine samples during treatment with Curaderm BEC5 showed no side effects 15, 17-20, 37-43.

Haematological (Table 4-1), biochemical (Table 4-2) and urinalytical parameters obtained from 62 patients prior to, during and after Curaderm BEC5 treatment indicated that the parameters remained within the population normal range.

Table 4-1: Blood Haematological constituents monitored before, during and after Curaderm BEC5 treatment.

White blood cells Red cell distribution width
Red blood cells Platelet count
Haemogloban Mean platelet volume
Haematocrit Heterophils
Mean corpuscular volume Lymphocytes
Mean corpuscular haemoglobin concentration Basophils
Mean corpuscular haemoglobin Monocytes

Table 4-2: Plasma Biochemical constituents monitored before, during and after Curaderm BEC5 treatment.

Sodium ion
Potassium ion
Chloride ion
Total CO2
Uric Acid
Urea nitrogen
Inorganic phosphate
Total Protein

There were no significant differences between before, during and after treatment in any of these parameters.

It was established that when a 1:1 mixture of solasonine and solamargine (the major components of BEC) was administered intravenously at a dose of 1.5 mg/kg/day over 4 hours the analyses of the pharmacokinetic data revealed that the biological half-life of solasonine was 5.57 ± 1.27 h and for solamargine this was 8.4 ± 2h. The clearance was 5.6 ± 1.6 L/h for solasonine and 3.0 ± 0.7 L/h for solamargine 44.

Unlike many other new drugs that meet the market place, we have established the mode of action of BEC. That is, we know how and why BEC selectively kills cancer cells but not normal cells. We have established that cell death occurs by apoptosis. Very interestingly, cancer cell death caused by BEC occurs while the cancer cells are “resting” and while they are “dividing”. This observation is in stark contrast to the other anticancer drugs that only kill cancer cells while they are dividing, they also kill normal cells when they too are dividing.

Mechanism of Action of BEC is Unique

We have now established that cancer cell death through interaction with BEC involves a biochemical process not exploited by the industry at the time.

Unlike established anticancer drugs, BEC is not anti-mitotic in its action. That is, it does not merely interfere with the cell division process. Rather the cell itself is killed through the interaction. Importantly, the mechanism of action incorporates cell lysis through disruption of the membrane of the lysosome thus releasing the contents of the lysosome within the cell which then kills the cell through a system similar to apoptosis.

Unlike other specific anticancer treatment such as matrix metalloproteinase inhibitors, BEC is toxic to cancer cells and the tumours are eradicated as opposed to merely being constrained. Unlike anti-angiogenics, cell death from BEC is rapid and not dependent upon “starving” the cancer cell.

Apart from the obvious advantage of providing a different “line of attack” against cancer (and the concomitant implications for multi-drug resistance), we have shown and now confirmed by independent other investigators, that BEC acts preferentially upon differentiated cells (cells transformed to cancer).

This may be compared to traditional “untargeted” cytotoxics (anticancer drugs) which equally affect normal cells, resulting in severe toxic reactions in fast growing tissues and associated adverse reactions such as nausea, infection (as a result of bone marrow suppression), hair loss, severe skin reaction and ulceration.

Importantly, traditional antineoplastic (anticancer drugs) are only effective at proliferating stages of cancer growth (when the cancer cells are dividing) whereas, BEC is effective at both proliferating and resting (non dividing) cancer cells.

Pharmacodynamic studies have determined that cancer cells have a specific receptor that recognizes and binds BEC. Normal cells do not have this receptor, or if so, in only minor quantities. So BEC does not attach itself significantly to normal cells.

BEC is then internalized into the cancer cells and kills the cancer cells as shown in figures 4-5 and 4-6. The receptor on the cancer cells have been characterized as a cell membrane glycoprotein 16, 18, 20-30, 34, 45-47.

Fig 4-5

Fig. 4-5: The results of cell culture and whole animal studies indicate that the mechanism of action of BEC involves the specific recognition of the sugar parts (in particular the sugar rhamnose) of the glycoalkaloids by specific receptors, lectins, located in the plasma membrane. Binding to these receptors, forming a complex of receptor-BEC results in endocytosis of the complex. Once inside the cell, the complex is taken up by the lysosomes (stomach of cell). The lysosome breaks up BEC and the alkaloid Solasodine is generated. Solasodine in turn causes the lysosome to rupture. The contents of the lysosome is spilt into the cell. The contents of the lysosome consists of many hydrolytic enzymes that can digest fats, proteins and carbohydrates. These enzymes then break down and digest the contents of the living cell which leads to sudden death of these affected cells. Malignant cells have greater abundance of these sugar receptors (lectins) than normal cells resulting in killing of cancer cells relative to normal cells.

Fig 4-6

Fig. 4-6: The glycoalkaloids causes the cytoplasm of the cancer cells to undergo dissolution, the nuclei contract and become dark staining (a), nuclei then enlarge (b), the chromatin (contents of nucleus) clumps (c), and finally the nuclei disintegrate (d). Only cellular debris is left after the interaction of the cancer cells with BEC (e). This cell death is characteristic of apoptosis which is also known as programmed cancer cell death.

An analogy of the unique mechanism of action of BEC is herewith
explained in simple English.

The BEC components are joined together as a sugar (glyco) part with an
alkaloid (solasodine) part. Imagine that cells are represented by
rooms with doors containing particular locks. A cancer cell is a room
with a specific door lock which is different than the door lock that
is on the normal (cell) room. The sugar (rhamnose) part of BEC may be
considered as a specific key and the alkaloid is a bomb. The key of
BEC only fits the lock and can open and enter the cancer cells. The
key of BEC does not fit and cannot unlock the door and thus can not
open or enter the normal cells. Once BEC has entered the cancer cell,
something in the cell causes the bomb (solasodine alkaloid) to explode
and the cancer cell is immediately killed. Because the bomb does not
get into the normal cells it cannot do harm to these cells.

Thus the uniqueness of BEC as opposed to all other anti-cancer drugs
is that BEC specifically only kills cancer cells without harming
normal cells!

Phase II Clinical Trials

A Phase II study marks the beginning of clinical trials on a specific, statistically determined number of patients to:

  • determine the efficacy of the compound for specific indications,
  • determine dosage tolerance and optimal dosage for future trials and
  • identify possible adverse effects and safety risks.

Specific Indications Studied


Actinic Keratosis

Malignant Skin Cancer

Basal Cell Carcinoma (BCC)
Squamous Cell Carcinoma (SCC)

Results of Phase II Clinical Trials with BEC

In all the clinical studies biopsies were taken before and after treatment with BEC formulations. This was done to ensure, not only clinically, but also histologically (microscopicaly) what skin cancer was treated, and to determine the effectiveness of BEC after the treatment was completed. On some occasions biopsies were taken during BEC therapy to determine by what methods BEC was killing the cancer cells.

The results of the Phase II clinical studies with 129 patients revealed that BEC in cream formulations was very effective for the chosen specific indications AK, BCC and SCC.

Patients tolerated high doses of BEC and it was determined that very low doses of BEC in the presence of keratolytic agents were optimal for treating the non melanoma skin cancers.

Fig 4-7

Fig. 4-7: Clinical and histological diagnosis of an SCC on a leg of a patient before treatment (lane A); during therapy (lane B); and site of treated SCC after completion of therapy (lane C). 1. clinical diagnosis; 2. histological diagnosis. Arrows indicate cancer cells dying during Curaderm BEC5 treatment (lane B; 2). The observation of this type of cell death caused by Curaderm BEC5 is similar to those obtained in cell culture studies.

The systemic adverse effects were non existent when blood chemistry, haematology and urine analysis were tested and compared before, during and after BEC therapy. No safety risks could be identified.

Fig 4-8

Fig. 4-8: Clinical diagnosis of a BCC on the nose of a patient before treatment with Curaderm BEC5 (1a), during therapy (1b) and site of treated BCC after completion of therapy (1c). Clinical progress of a BCC close to the eye of the patient before treatment (2a), during therapy (2b), and site of treated BCC after completion of therapy with Curaderm BEC5 (2c).

Local adverse effects were limited to local skin irritation and erythema (reddening of the skin). Some patients experienced some pain at the site of application for a short duration 15, 17-20,37-43.

Fig 4-9

Fig. 4-9: Histological analysis of a BCC before Curaderm BEC5 therapy showing the deep infiltrated cancer cells well within the dermis (a); after Curaderm BEC5 therapy no cancer cells are present (b).

Phase III Clinical Trials

The results of Phase III trials determined that BEC in cream formulations were effective and the safety profile was very acceptable.

Curaderm BEC5 and Phase III Clinical Studies (232 patients)

BEC was now ready to undergo a more extensive clinical trial. Curaderm BEC5 was chosen for the Phase III trials. Single and randomized double-blind placebo controlled studies were done on patients with lesions as described with the Phase II studies. A placebo is an inactive cream (in our case the same cream formulation but without the BEC) that has no treatment value. Experimental treatments are compared with placebos to assess the experimental treatment’s effectiveness. The Phase III studies were done in Australia and independent multi-centre hospitals in the United Kingdom. Before the clinical studies commenced appropriate protocols were assessed to determine the appropriate execution of the clinical trials. In the United Kingdom the protocol was approved by the Medical Control Agency (MCA) for the multi-centre studies. A protocol is a carefully designed study plan to safeguard the health of the participants as well as answer specific research questions.

The results of the Phase III trials determined that Curaderm BEC5 produced success rates of 78% when Curaderm BEC5 was applied twice daily under occlusive dressing for 8 weeks. If the treatment regime was extended to 12 weeks the success rates were virtually 100%. Only local skin irritation and erythema were observed as adverse reactions. Therefore the treatment with Curaderm BEC5 was considered to be a safe therapy.

Success was defined as zero presence of non melanoma skin cancers after histological examination of samples extracted from the lesion site by punch biopsy. In addition, treated patients were followed up for over 5 years post treatment and it was determined that there were no recurrences of the treated lesions! 18-20, 41-43, 48-53 Figures 4-7 to 4-11 show cases which have been followed up 5 years post treatment.

Fig 4-10

Fig. 4-10: Large BCC on the temple of a woman (a). This BCC had been surgically removed and skin grafts applied on two previous occasions only to return. Four weeks treatment with Curaderm resulted in full regression (b). Note the cosmetic result. The clinical diagnosis was confirmed histologically by punch biopsy (c). After completion of the therapy histopathology determined that no residual cancer was present (d). Clinical assessment 5 years post treatment revealed that there was no recurrence.

Fig 4-11

Fig. 4-11: SCC on the nose of a patient before (a), during (b) and after Curaderm treatment (c). Curaderm was applied for 5 weeks. Note the depth of the cancer as cartilage was exposed during treatment. The clinical diagnosis was confirmed histologically by punch biopsy (d). After completion of the therapy histopathology determined that no residual cancer was present (e). Clinical assessment 5 years post treatment revealed that there was no recurrence.

Phase IV or Post-Marketing Studies

These studies are done to further confirm and describe clinical benefit of Curaderm BEC5 and yield additional information including risks and optimal use. Post-launch safety surveillance is designed to detect any rare or long-term adverse effects over a much larger patient population and timescale than was possible during the initial clinical trials.

Phase IV trials are important as they detect any rare or long-term adverse effects. Such adverse effects have resulted in the withdrawal or restriction of a drug, recent examples include cerivastatin (Baycol, Lipobay), troglithzone (Rezulin) and rofecobix (Vioxx).

Registration of adverse effects when 50,000 patients had used Curaderm BEC5 resulted in only two adverse effects documented over a ten year period with the Therapeutic Goods Administration (TGA) in Australia. Both documented adverse effects were dermatitis at the site of Curaderm BEC5 application. Cessation of Curaderm BEC5 application resulted in remission of the dermatitis. These observations secure Curaderm BEC5 treatments as having an exceptional safety profile 50, 54.

Following are some patient cases (figures 4-12 and 4-13) that have been treated with Curaderm BEC5 at the Phase IV clinical stages.

Fig 4-12

Fig. 4-12: Large BCC on the leg (a). Note how rapid the cancer was being destroyed by Curaderm during treatment (b - d) and how rapid the wound healed after 5 weeks of Curaderm therapy (e). The clinical diagnosis was confirmed histologically by punch biopsy (f). After completion of the therapy histopathology determined that no residual cancer was present (g). Clinical assessment 5 years post treatment revealed that there was no recurrence.


It can therefore be concluded that Curaderm BEC5 has been critically evaluated, and when compared to many drugs that are currently marketed, is far superior in safety and efficacy.

Curaderm BEC5 has met all the requirements regarding, research, pre-clinical, and clinical studies to enable its rightful place acceptance by health professionals and public as an excellent treatment for non melanoma skin cancers.

Curaderm BEC5 is the treatment of choice for non melanoma skin cancers.

Fig 4-13

Fig. 4-13: A large SCC (approximately 8cm x 6cm) on the shoulder of a patient before (a), during (b) and after (c) treatment with Curaderm. After 10 weeks the tumour was completely healed. The clinical diagnosis was confirmed histologically by punch biopsy (d). After completion of the therapy histopathology determined that no residual cancer was present (e). Clinical assessment 5 years post treatment revealed that there was no recurrence.