The present disclosure relates to an anticancer composition and a process for preparing the same. ABBREVIATIONS

LLC: Leucas linifolia crude extract

LLCs: Chloroform extract of successive extraction of LLC (non polar to polar) LLCM: Methanol treated LLCs LLCCE: Eluant of LLCM from silica gel column LLHPLC: Eluant collected from LLCCE by C 18, RPHPLC column B16F10: is a mouse melanoma cell line. A375: is a human malignant melanoma cell line.

MCF-7: MCF-7 is a breast cancer cell line and is the acronym of Michigan Cancer Foundation-7, where the cell line was established. MDA-MB-231: MD Anderson-Metastatic Breast-231refers to a Human breast cancer cell line.

U87: is a human primary glioblastoma cell line formally known as U-87 MG. DEFINITIONS

As used in the present disclosure, the following terms are generally intended to have the meaning as set forth below, except to the extent that the context in which they are used indicate otherwise.

IC5 ₀ : The half maximal inhibitory concentration (IC5 ₀ ) is a measure of the effectiveness of a substance in inhibiting a specific biological or biochemical process (or component of a process, i.e., an enzyme, cell, cell receptor or microorganism) by half. MTT assay: The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay is a colorimetric assay for assessing cell metabolic activity.

Parenteral preparation: Parenteral preparations are sterile preparations containing one or more active ingredients intended for administration by injection, infusion or implantation into the body. They are packaged in either single-dose or multidose containers.

BACKGROUND

Cancer, also known as a malignant tumour or malignant neoplasm, is a group of diseases involving abnormal cell growth, due to the loss of contact inhibition. These abnormal cells divide in an uncontrolled way and generally have a potential to invade or spread to other healthy parts/tissues of the body. These abnormal cells when spread to other parts of the body, this process is called as metastasis.

Particularly, breast cancer is a leading cause of morbidity and mortality among women, because breast cancer has a poor prognosis, and women with metastatic breast cancer have a limited time for survival. Conventionally, only three treatments for cancer, i.e., surgery, radiation, and chemotherapy, are used for years with very little long-term success. Surgery is generally the first line of treatment to try for most types of cancer, as solid tumours can usually be surgically removed. These conventional treatments can affect the body systems, such as the blood circulation, lymphatic and immune systems, and the hormone system. Since these conventional treatments also involve the use of powerful cancer-killing medication and/or controlled use of high-energy X-rays, they have many side effects, mainly damaging the normal healthy cells, anemia, etc., and are also expensive. Moreover, alternative cancer treatments (like herbal treatments) are less expensive than surgery, radiation, and chemotherapy and have fewer unwanted side effects. However, the significant side effects and the potential for the development of treatment resistance combined with limited survival benefit associated with conventional treatments has prompted the use of alternative cancer treatments, like herbal medicines. Moreover, due to breast cancer's increasing incidences and alarming mortality rates, there still remains a need for such alternative therapies for alleviating the symptoms of breast cancer, which are economical, safe, efficacious, non-invasive, and a natural solution, which eliminates the need for conventional expensive drugs and their associated side effects caused due to prolonged daily use.

OBJECTS

Some of the objects of the present disclosure, which at least one embodiment herein satisfies, are as follows:

It is an object of the present disclosure to ameliorate one or more problems of the prior art or to at least provide a useful alternative.

It is an object of the present disclosure to provide an anticancer composition which is safe with minimal side effects. It is another object of the present disclosure to provide an anticancer composition which is effective, and can be taken with other medicines without any side effects.

It is yet another object of the present disclosure to provide an anticancer composition which is effective in alleviating the symptoms of breast cancer.

Other objects and advantages of the present disclosure will be more apparent from the following description, which is not intended to limit the scope of the present disclosure.

SUMMARY

In an embodiment of the present disclosure, there is provided an anticancer composition for alleviating the symptoms of breast cancer comprising an urticic acid methyl ester and at least one pharmaceutically acceptable carrier. The urticic acid methyl ester is derived from Leucas linifolia. The anticancer composition is suitable for parenteral administration such as intramuscular, intravenous, and subcutaneous injection. The anticancer composition further comprises a suspending agent, a solubilizer, a preservative, a buffer, an isotonizing agent, and a stabilizer.

The present disclosure also provides a method for preparation of the anticancer composition. The present disclosure also provides a method for treating breast cancer in a mammal comprising parenterally administering effective amount of an anti-cancer composition to the mammal. BRIEF DESCRIPTION OF THE ACCOMPANYING DRAWING

The present disclosure will now be described with the help of the accompanying drawing, in which:

Figure la illustrates the cytotoxic effect of LLC crude extract on MCF-7 and MDA-MB-231 cell lines; wherein curve 1 represents MDA-MB-231 cell line and curve 2 represents MCF-7 cell line and Figure lb illustrates the cytotoxic effect of doxorubicin (positive control)on MCF-7 and cisplatin (positive control) on MDA-MB-231 cell lines; wherein curve 3 represents the cytotoxic effect of doxorubicin (positive control) on MCF-7 cell line and curve 4 represents the cytotoxic effect of cisplatin (positive control) on MDA-MB-231 cell line; Figure lc illustrates the cytotoxic effect of tamoxifen on MDA-MB-231 cell line;

Figure 2 illustrates the protective effect of the herbal anticancer compound against H2O2 induced damage in Human RBC; wherein curve 5 represents LLC and curve 6 represents ascorbic acid (positive control);

Figure 3a illustrates the cytotoxic effects of LLCM extracts on B16F10, A375 and U87 cell lines; wherein curve 16 represents B16F10 cell line, wherein curve 17 represents A375 cell line and wherein curve 18 represents U87 cell line; Figure 3b illustrates the cytotoxic effects of LLCCE extracts on B 16F10, A375 and U87 cell lines; wherein curve 19 represents B 16F10 cell line, wherein curve 20 represents A375 cell line and wherein curve 21 represents U87 cell line; and Figure 3c illustrates the cytotoxic effects of positive control (Cisplatin) on B 16F10, A375 and U87 cell lines; wherein curve 22 represents B 16F10 cell line, wherein curve 23 represents A375 cell line and wherein curve 24 represents U87 cell line.

Figure 4 illustrates the cytotoxic effects of LLCM, LLCCE extracts and positive control (cisplatin) on B16F10, A375 and U87 cell lines; wherein curve 7 represents LLCM, curve 8 represents LLCCE and curve 9 represents cisplatin; Figure 5 illustrates the effect of seasonal variation on the cytotoxicity of LLCM; wherein curve 10 represents <ICso, curve 11 represents IC5 ₀ , curve 12 represents >ICso;

Figure 6 illustrates the effect of temperature on the cytotoxicity of LLCM against MDA-MB- 231 cell line; wherein curve 13 represents <ICso, curve 14 represents IC5 ₀ , curve 15 represents >ICso; Figure 7 illustrates the effect of storage period on the cytotoxicity of the LLC crude extract against MDA-MB-231 cell line; and

DETAILED DESCRIPTION

Breast cancer is one of the most common cancers and is often identified as being the second cause of cancer deaths in women. The conventional therapies for treating breast cancer include surgery, hormone therapy, radiation, and chemotherapy. These conventional therapies result in undesirable side effects and are also expensive. The available alternative therapies for cancer are not reliable and do not provide satisfactory results. Therefore, the present disclosure envisages an herbal anticancer composition which is effective, safe and does not suppress the immune system for alleviating the symptoms of breast cancer.

In an aspect of the present disclosure, there is provided an anticancer composition. The composition comprises urticic acid methyl ester, and at least one pharmaceutically acceptable carrier. The urticic acid methyl ester is derived from Leucas linifolia. The urticic acid methyl ester is used in an amount in the range of 1 to 30 wt% of the anticancer composition. Leucas linifolia is native to the Indian sub-continent, but also grows in Pakistan, Sri-Lanka and Bangladesh. The plant, as used in the present disclosure has been sourced from outside India.

In the present disclosure, the urticic acid methyl ester is derived from the plant material selected from various parts of the plant such as rhizomes, stems, flowers, leaves, and fruits. Typically, the plant part used are leaves. Typically, the leaves of Leucas linifolia as used in the present disclosure are dried leaves.

In an embodiment of the present disclosure, the anticancer composition is suitable for parenteral administration.

In an embodiment of the present disclosure, the pharmaceutically acceptable carrier is at least one selected from the group consisting of water, and ethanol. The pharmaceutically acceptable carrier is suitable for intramuscular, intravenous, and subcutaneous injection. The pharmaceutically acceptable carrier is used in an amount in the range of 50 to 99 wt% of the anticancer composition. The anticancer composition further comprises a suspending agent, a solubilizer, a preservative, a buffer, an isotonizing agent, and a stabilizer.

In an embodiment of the present disclosure, the suspending agent is at least one selected from the group consisting of sodium carboxymethyl cellulose, methyl cellulose, gelatin, and polyvinyl pyrrolidone. The suspending agent is used to avoid cake formation in the anticancer composition. The amount of suspending agent used is in the range of 0.5 to 10 wt% of the anticancer composition.

The solubilizer is at least one selected from the group consisting of lecithin, polyoxyethylene sorbitan monolaurate, polyoxyethylene sorbitan monooleate, and sorbitan trioleate. The solubilizer is used to reduce surface tension between the particles and the pharmaceutically acceptable carrier that increases the solubility of the ingredients of the anticancer composition in pharmaceutically acceptable carrier. The amount of solubilizer used is in the range of 0.05 to 0.5 wt% of the anticancer composition.

The preservative is at least one selected from the group consisting of benzalkonium chloride, methyl paraben, propyl paraben, and benzyl alcohol. The amount preservative used is in the range of 0.05 to 2 wt% of the anticancer composition.

The buffer is at least one selected from the group consisting of sodium benzoate, potassium phosphate, sodium phosphate, citric acid, sodium tartarate, lactic acid, and sodium citrate. The amount of buffer used is in the range of 0.05 to 2 wt% of the anticancer composition. The preservatives and buffers are used to provide the stability to the anticancer composition.

The isotonizing agent is at least one selected from the group consisting of glycerine, mannitol, and amino ethyl sulfonic acid. The amount of isotonizing agent used is in the range of 0.05 to 5 wt% of the anticancer composition.

The stabilizer is at least one selected from the group consisting of inositol, potassium pyrosulfite, sodium gluconate, and triethanolamine. The amount of stabilizer used is in the range of 0.05 to 5 wt% of the anticancer composition.

In one embodiment of the present disclosure, there is provided a process for preparing the anticancer composition. The urticic acid methyl ester and solubilizer are added in the first portion of at least one pharmaceutically acceptable carrier to obtain a first mixture. Further, separately adding a suspending agent, a isotonizing agent and a stabilizer in the second portion of at least one pharmaceutically acceptable carrier to obtain a second mixture. The first mixture is added to the second mixture with continuous stirring, followed by the addition of a preservative and buffers to obtain the anticancer composition. The anticancer composition is then sterilized to obtain sterilized anticancer composition. The urticic acid methyl ester of the present disclosure is isolated from the leaves of Leucas linifolia. The process includes collecting and washing the fresh leaves of Leucas linifolia with distilled water, followed by drying for approximately 15 days. Further the dried leaves are cut into small pieces and are powdered and stored in air tight containers at 4 °C until further use to avoid any change/degradation, to preserve the phytochemicals and to prevent any contamination of the powder. The crude extracts are obtained by macerating the stored powder in an extraction vessel with at least one organic solvent. This extract is further subjected to a gradient extraction using methanol. At each step of extraction, cytotoxicity is tested by MTT assay against MDA-MB-231 cell line, and the effective fraction (the fraction which showed cytotoxicity) is taken to the next step of purification, while the non-active fractions are discarded. The effective fraction is then used to prepare the anticancer composition.

The organic solvent used for maceration of crude extract containing urticic acid methyl ester is at least one selected from the group consisting of chloroform, n-hexane, acetonitrile, ethyl acetate, ethanol, and methanol. In another aspect of the present disclosure, there is provided a method for treating breast cancer in a mammal comprising parenterally administering effective amount of an anti-cancer composition to the mammal. The composition comprises urticic acid methyl ester and at least one pharmaceutically acceptable carrier. The urticic acid methyl ester is derived from Leucas linifolia. In an embodiment of the present disclosure, the anticancer composition is administered at a dose ranging from 20 to 300 mg/kg of bodyweight/day.

The present disclosure is further described in light of the following experiments which are set forth for illustration purpose only and not to be construed for limiting the scope of the disclosure. The following experiments can be scaled up to industrial/commercial scale and the results obtained can be extrapolated to industrial scale. EXPERIMENTS:

Experiment 1: Extraction and purification of the anticancer compound (Urticic acid methyl ester) and testing for anticancer activity:

10 g of the powder was macerated in 100 ml chloroform for 48 hours with constant stirring to obtain LLC. LLC was then extracted successively using 10 ml of n-hexane and 10 ml of chloroform to obtain LLCs. LLCs were then treated with 10 ml of methanol, incubated at 28 °C for 1 hour for enabling the precipitation, followed by centrifugation at 1000 rpm for 10 minutes to obtain the supernatant, i.e., LLCM. The supernatant (LLCM) was used as it showed cytotoxicity against the MDA-MB-231 cell line. Further LLCM was passed through a silica gel column and eluted with methanol : water (80:20% v/v) to obtain LLCCE. Four fractions of 6 ml each of LLCCE were then collected. These fractions of LLCCE were then passed through CI 8, Reverse Phase High Pressure Liquid Chromatography (RPHPLC) to obtain LLHPLC. HPLC analysis was carried out to obtain a single peak with retention time 2.85 mins. The crude extracts, after each purification step, were tested for their anticancer potential by MTT assay at different concentrations (1.57 μg/ml tolOO μg/ml) and the % cell death was calculated. The cytotoxic potential of the extract was measured in terms of IC5 ₀ . The crude extracts showed effective cytotoxicity at an ICsovalue of 29.2 ± 1.31 μg/ml and 40.0 ± 1.29 μg/ml against MCF-7 and MDA-MB-231 cell lines respectively (Figure la). Cisplatin (positive control) gave an IC5 ₀ value of 0.5 ± 0.1 μg/ml and Doxorubicin (positive control) gave an IC5 ₀ value of 1.09 ± 0Λμg/mί (Figure lb). Figure lc depicts the cytotoxic effects of tamoxifen on MDA-MB-231 cell line with the concentration of the tamoxifen ^g/ml) on x- axis and % cell death on Y-axis. Concentration of tamoxifen ^g/ml): 0.63 μg/ml, 1.25 μg/ml, 2.5 μg/ml and 5 μg/ml. IC5 ₀ values were calculated from a graph plotted with concentration of tamoxifen on x-axis and % cell death on Y-axis. (IC5 ₀ - Concentration of the extract at which 50% of the cell death is seen). Tamoxifen gave an IC5 ₀ value of 42.7 ± 0^g/ml (Figure lc).

After each step of purification, the IC5 ₀ values of the extract decreased, indicating effective cytotoxicity against MDA-MB-231 cell line. The purified compound was effective at an IC5 ₀ value of 6.1 ± 2.89 μg/ml as summarised in Table 1. Table 1: IC5 ₀ values of the extract during purification against MDA-MB-231 cell line.

Figure la depicts the cytotoxic effect of LLC crude extract on MCF-7 and MDA-MB-231 cell lines respectively. The concentration of the LLC extract tested was 200 μg/ml, 100 μg/ml, 50 μg/ml, 25 μg/ml and 12.5 μg/ml. Concentration of cisplatin tested was 10 μg/ml, 5 μg/ml, 2.5 μg/ml, 1 μg/ml and 0.5 μg/ml. Concentration of tamoxifen tested was 0.63 μg/ml, 1.25 μg/ml, 2.5 μg/ml and 5 μg/ml. The IC5 ₀ values were calculated from the graph (Figure la, figure lb and figure lc) plotted with concentration of the extract on x-axis and % cell death on Y-axis. Experiment 2: Toxicity of the anticancer compound against normal cells:

The anticancer compound (Urticic acid methyl ester) was tested against a normal cell line, i.e., Human dermal fibroblasts (HDF) cell line by MTT assay. The assay was performed as per the procedure described in Denizot and Lang, 1986; Mossman, 1983. It is a colorimetric assay based on the cleavage of MTT (3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), a soluble yellow colored tetrazolium salt to a purple colored formazan by the mitochondrial enzyme succinate dehydrogenase which was quantified spectrophotometrically at 570nm. Cells were then plated in a 96 well flat bottom microtiter plates at a density of 5 x 10 ⁴ cells per well and were cultured in DMEM (Dulbecco's Modified Eagle Medium) medium at 37 °C, in 5 % CO2 atmosphere, for 24 hours, to allow the cell adhesion. After 24 hours, when partial monolayers were formed, the medium was removed and the cells were treated with different concentrations of LLCM and LLCCE extracts (3.13 μg/ml, 6.25 μg/ml, 12.5 μg/ml, 25 μg/ml, 50 μg/ml and 100 μg/ml) for 48 hours. Cells without any treatment were maintained as negative control. After the treatment, the culture media in the wells was discarded and 100 μΐ of freshly prepared MTT (1 mg/ml PBS) was added to each well. The plates were shaken gently and incubated at 37 °C in 5 % C(¾ atmosphere for 4 hours. After 4 hours, the supernatant was removed and the formazan crystals formed in the cells were solubilized by addition of 100 μΐ of DMSO. The absorbance was read using a micro-plate reader (Bio-Tek, ELX-800 MS) at 570 nm. The assay was done in triplicate for each of the extract.

The percentage growth inhibition was calculated using the formula below:

% Growth inhibition = (Control absorbance - test absorbance) x 100

(Control absorbance)

No cytotoxicity was observed with the crude extracts, however after purification, 6.03 % cell death was observed with the highest concentration tested i.e., 100 μg/ml towards HDF cell lines as summarised in Table 2. LLCM at the highest concentration tested i.e., 100 μg/ml showed 92.58% cell death towards MDA-MB-231 cell line and LLCCE at the highest concentration tested i.e., 100 μg/ml showed 95.51% cell death towards MDA-MB-231 cell line.

Table 2: Toxicity of LLCM and LLCCE extracts on HDF & MDA-MB-231 cell lines by

MTT assay

Cytotoxicity (%)

Name of the extract

HDF MDA-MB-231

LLCM (100 μ^ηιΐ) 0% (no cell death) 92.58 + 3.2 LLCCE (ΙΟΟ μ^ιηΙ) 6.03 + 1.12 95.51 + 2.7

Experiment 3: Toxicity of the anticancer compound against human RBC's:

The anticancer compound (Urticic acid methyl ester) was tested against human RBC's. The highest concentration tested was 200 μg/ml but no haemolysis was observed (Table 3). The anticancer compound (Urticic acid methyl ester) was also protective against ¾(¾ induced RBC haemolysis at a concentration of 50 μg/ml (Figure 2). Figure 2 depicts the protective effect of the anticancer compound against ¾(¾ induced damage in Human RBC. LLCM extracts were tested for protective effect against ¾(¾ induced damage in Human RBC at different concentrations (5 μg/ml, 10 μg/ml, 25 μg/ml, 50 μg/ml and 100 μg/ml) and the % scavenging activity was calculated. Ascorbic acid was used as the standard. The extract was able to protect the RBC's from haemolysis upto a concentration of 50 μg/ml, but hemolysis was seen at higher concentrations.

The anticancer compound did not induce haemolysis against human RBC's at the highest concentration tested, i.e. 200 μg/ml. Table 3 summarizes the % hemolysis of the LLCCE extracts against the Human RBC at different concentrations (12.5 μg/ml, 25 μg/ml, 50 μg/ml, 100 μ^πύ and 200 μ^πύ).

Table 3: Toxicity of the anticancer compound by hemolysis assay

Cone, of the extract Hemolysis (%) of Human ^g/ml) RBC's

200 -1.24

100 -1.22

50 -1.14

25 -1.30

12.5 -1.54 Experiment 4: Effectiveness of the anticancer compound against other cancer cell lines:

The anticancer compound (Urticic acid methyl ester) was tested for its effectiveness against other cancer cell lines by MTT assay. Cells were initially treated with different concentrations of LLCM and LLCCE extracts (6.25 μg/ml, 12.5 μg/ml, 25 μg/ml, 50 μg/ml and 100 μg/ml) with cisplatin as the positive control for 48 hours (Figures 3a, 3b and 3c). Cells without any treatment were maintained as negative control. The experiment was done in triplicate and the mean ± SD of % growth inhibition were taken for plotting the graphs. The IC5 ₀ values were determined from the graphs (Figures 3a, 3b and 3c) plotted with % growth inhibition vs. concentration of the crude extracts and expressed in μg/ml. The anticancer compound exhibited effective cytotoxicity against various other cancer cell lines as depicted in Figure 4. The efficacy of the anticancer compound was tested in U87 (human glioblastoma), A375 (human melanoma), B 16F10 (mouse melanoma) and compared with MDA-MB-231 cell line.

The IC5 ₀ values varied with the type of cell line used in the following order: MDA-MB-231 (6.1 ± 2.89μg/ml)> A375 (11.8 ± 3.1 μg/ml)> B 16F10 (22.68 ± 1.8 μg/ml)> U87 (32.1 ± 5^g/ml), as shown in Figure 4. Figure 4 depicts the cytotoxic effects of LLCM, LLCCE extracts and the positive control (cisplatin) on B16F10, A375 and U87 cell lines.

Experiment 5: Effectiveness of the extract from leaves collected in different seasons of the year:

The effectiveness of the extract from leaves collected in different seasons of the year was also tested at varying concentrations (6.25 μg/ml, 12.5 μg/ml and 25 μg/ml) against MDA-MB- 231 cell lines by MTT assay. The three concentrations tested were < IC5 ₀ value, IC5 ₀ value and >IC5o value. % cell death was derived and plotted against time of collection of leaves. The extract (LLCM), was prepared as disclosed herein above, from the leaves of Leucas linifolia collected during the months of August, December and May gave an IC ₅₀ value of 12.15 ± 2.8 μg/ml, 18.55 ± 4.2 μg/ml and 46.26 ± 6.3 μg/ml respectively, as depicted in Figure 5. Seasonal variation influenced the cytotoxicity of the LLC extract against MDA- MB-231 cell line. The activity in the month of May decreased in comparison to the activity during August and December. Experiment 6: Effectiveness of the extract incubated at various temperatures for an hour before treatment of the cell lines: The anticancer compound (Urticic acid methyl ester) was tested for its effectiveness at various temperatures (4 °C, 37 °C, and 60 °C) before treatment of the cell lines by MTT assay. The cytotoxic efficacy was tested on MDA-MB-231 cell line at varying concentrations (6.25 μg/ml, 12.5 μg/ml and 25 μg/ml) by MTT assay. The three concentrations tested were < IC5 ₀ value, IC5 ₀ value and >ICso value. % cell death was plotted against varying temperature. The anticancer compound (Urticic acid methyl ester) was incubated at different temperatures for an hour and then used against different cell lines. Figure 6 depicts the cytotoxic activity of the LLCM at different temperatures against MDA-MB-231 cell line. At 4 °C and 37 °C the IC5 ₀ values were found to be 14.7 ± 3.2 μg/ml and 15.4 ± 1.9 μg/ml respectively. With the increase in temperature to 60 °C, no cell death was observed. With the increase in the temperature i.e., at 60 °C LLC did not show any cytotoxicity against MDA-MB-231 cells indicating the anticancer compound is active only at low and room temperatures.

Experiment 7: Long term stability of the extract as mentioned herein above:

The anticancer compound (Urticic acid methyl ester) was tested for its long term stability by MTT assay as mentioned above. IC5 ₀ values of the crude extract at 0, 6, 12, 18, 24 and 30 months have been plotted in Figure 7.

The anticancer compound (Urticic acid methyl ester) was stored for a span of 0 to 30 months. The storage period of the extracts (0-30 months) did not have any effect on the cytotoxic activity against MDA-MB-231 as shown in Figure 7. Figure 7 depicts the IC5 ₀ values of the anticancer compound at 0, 6, 12, 18, 24 and 30 months. Experiment 8: An anticancer composition in accordance with the present disclosure:

The anticancer composition was prepared by using the following ingredients as given in Table- 1.

Table 1

The urticic acid methyl ester and polyoxyethylene sorbitan monooleate were added in the first portion of ethanol (10.6 mg) and water (25 mg) to obtain a first mixture. Further, separately adding polyvinyl pyrrolidone, mannitol and inositol in the second portion of ethanol (10 mg) and water (25 mg) to obtain a second mixture. The first mixture is added to the second mixture with continuous stirring, followed by the addition of methyl paraben, propyl paraben and sodium benzoate to obtain the anticancer composition. The anticancer composition is then sterilized using MF-milipore filter to obtain sterilized anticancer composition.

TECHNICAL ADVANCEMENTS The present disclosure described herein above has several technical advantages including, but not limited to, the realization of:

- an herbal anticancer composition which alleviates the symptoms of breast cancer without affecting the normal cells; and - an herbal anticancer composition which is safe, effective, and can be taken with other medicines without any side effects.

The embodiments as described herein above, and various features and advantageous details thereof are explained with reference to the non-limiting embodiments in the description. Descriptions of well-known aspects, components and molecular biology techniques are omitted so as to not unnecessarily obscure the embodiments herein.

The foregoing description of specific embodiments so fully reveal the general nature of the embodiments herein, that others can, by applying current knowledge, readily modify and/or adapt for various applications of such specific embodiments without departing from the generic concept, and, therefore, such adaptations and modifications should and are intended to be comprehended within the meaning and range of equivalents of the disclosed embodiments. It is to be understood that the phraseology or terminology employed herein is for the purpose of description and not of limitation. Therefore, while the embodiments herein have been described in terms of preferred embodiments, those skilled in the art will recognize that the embodiments herein can be practiced with modification within the spirit and scope of the embodiments as described herein. Further, it is to be distinctly understood that the foregoing descriptive matter is to be interpreted merely as illustrative of the disclosure and not as a limitation.

Having described and illustrated the principles of the present disclosure with reference to the described embodiments, it will be recognized that the described embodiments can be modified in arrangement and detail without departing from the scope of such principles.

While considerable emphasis has been placed herein on the particular features of this disclosure, it will be appreciated that various modifications can be made, and that many changes can be made in the preferred embodiment without departing from the principles of the disclosure. These and other modifications in the nature of the disclosure or the preferred embodiments will be apparent to those skilled in the art from the disclosure herein, whereby it is to be distinctly understood that the foregoing descriptive matter is to be interpreted merely as illustrative of the disclosure and not as a limitation.