KR100892764B1 - Modified ginsenoside mixture which has selective anti-lung cancer activity - Google Patents

Abstract

The present invention relates to a composition exhibiting an anticancer effect containing ginsenosides, a glycoside of the pharmacologically active ingredient of ginseng as an active ingredient. Ginsenoside composition H-2 according to the present invention is a ginsenoside Rg3, Rh1, Rh2, PPT and isomers prepared using ginsenosides (Rb1, Rg1, etc.) extracted from ginseng and ginseng processed products It is an oral combined ginsenoside anticancer agent having a strong selective inhibitory activity against lung cancer as a cenoside composition.

Ginsenosides, glycosides, lung cancer

Description

Ginsenoside composition for treating lung cancer {Modified ginsenoside mixture which has selective anti-lung cancer activity}

1 is a result of analyzing the ginsenoside composition H-2 of the present invention by HPLC.

2 is a result of analyzing the ginsenoside composition H-2 of the present invention by TLC.

The present invention relates to an anticancer agent composition comprising ginsenosides, which are glycosides, as pharmacologically active ingredients of ginseng. Ginsenoside composition H-2 according to the present invention is a ginsenoside Rg3, Rh1, Rh2, PPT and isomers prepared using ginsenosides (Rb1, Rg1, etc.) extracted from ginseng and ginseng processed products It is an oral combined ginsenoside anticancer agent having a strong selective inhibitory activity against lung cancer as a cenoside composition.
As used herein, "ginsenoside Rb1" means [20-O- [β-D-glucopyranosyl (1 → 6) -β-D-glucopyranosyl] -3-O- [β-D-glucopyranosyl]. (1 → 2) -β-D-glucopyranosyl] -20 (S) -proctopanoparanadiol], and “ginsenoside Rd” is [20-O- [β-D-glucopyranosyl]- 3-O- [β-D-glucopyranosyl (1 → 2) -β-D-glucopyranosyl] -20 (S) -proptophanacanadiol] and “ginsenoside Re” is 20-O -[β-D-glucopyranosyl] -6-O- [α-L-rhamnopyranosyl- (1 → 2) -β-D-glucopyranosyl] -20 (S) -proctopanoxatriol , "Ginsenoside Rg1" refers to 20-O- [β-D-glucopyranosyl] -6-O- [β-D-glucopyranosyl] -20 (S) -protophanacanatriol, Cenoside Rg2 "refers to 6-O- [α-L-rhamnopyranosyl- (1 → 2) -β-D-glucopyranosyl] -20 (S) -proctoponaxatriol," Ginsenoside Rg3 "3-O- [β-D-glucopyranosyl (1 → 2) -β-D-glucopyranosyl] -20 (S) -proctopanoparanadiol," ginsenoside Rh1 "is 6- O-β-D-glucose Rannosyl-20 (S) -proctopanoxatriol, "ginsenoside Rh2" refers to 3-O-β-D-glucopyranosyl-20 (S) -proctopananaxadiol, "ginsenoside PPT "was used to mean 20 (S) -proctopanoxatriol. In addition, the ginsenosides are also abbreviated as "Rb1", "Rd", "Re", "Rg1", "Rg2", "Rg3", "Rh1", "Rh2", "PPT", respectively. . The ginsenoside name is a common name that is widely known to those skilled in the art.

For the development of new anti-cancer therapies, extensive research is being conducted on natural products and processed products modified from them. Ginseng and its processed red ginseng have long been used as a preventive and therapeutic agent for various diseases (Shibata, J. korean Med Sci 2001; 16 (suppl): S28), and ginsenoside, an active ingredient, also has anticancer activity. Ginsenoside Mc (ginsenoside Mc; registered patent 0164266), ginsenoside Rh2 (patent publication 89-28759, Japan), ginsenoside Rg5 (ginsenoside Rg5; registered patent 10-0183448) Although it has been reported to have a therapeutic effect as a single or a main ingredient, it has been difficult to produce ginsenosides of a single component, and thus, it was not possible to produce a drug due to mass production, and there was no conviction that a single component of ginsenoside was superior to the complex ginsenosides. Because of the difficulty in drugization.

In addition, the ginsenoside composite material that has been studied so far has a lot of problems in quality control including reproducibility because there are too many ingredients other than ginsenoside.

In addition to anticancer effects, ginsenosides have an immune enhancing effect ( ginsenoside Rg1 / Okamura N et al. Biol. Pharm. Bull. 17 (2), 270 (1994)) and anti-fatigue ( ginsenoside Rg1 / Saito H et al. Japan J Pharmacology, 24, 119 (1974), ginsenoside Rg1 / Yoshimatsu H et al. Physiology and Behavior, 53 (1), 1 (1993), ginsenoside Rd, Re / Hiai S et al. Chem Pharm. Bull. 31, 168 (1983)), protein synthesis promoting action ( ginsenoside Rb1 / Zhang JT et al. Acta Pharmaceutica Sinica 23 (1), 12, (1988)) have. Therefore, the ingestion of ginsenosides acts as an adjuvant to increase anti-cancer activity indirectly, such as in vivo immunization. In addition, when taking ginsenosides in the form of natural products (Rb1, Rg1, Rd, Rb2, Rc, Rf), new ginsenosides (Rg3, Compound K, Rh1, Mc, which are decomposed by digestive enzymes and intestinal microorganisms and have strong anticancer activity) , Y, F2, etc.) are produced to show anticancer effects (Planta Med 62 (1996) 457). However, these anticancer effects vary depending on the presence and activity of intestinal microorganisms that produce digestive enzymes, so the expected value for anticancer effects is not positive (Planta Med 63 (1997) 439).

Accordingly, an object of the present invention is to overcome the problems of conventional drugs or health supplements such as anticancer agents using single or multi-component ginsenosides, and to provide a more effective ginsenoside-containing anticancer agent.

For the preparation of a compound ginsenoside strong anti-cancer activity, the present invention is the total ginsenoside content of 85% or more, as a single component composition Rb1, Rg1, Rd, Re, Rg3, Rh1, Rh2, PPT, △ ²⁰ - ginsenoside Side Rg3 (double bond conformation at the carbon position of ginsenoside structure No. 20 is the optical isomer of ginsenoside Rg3, and Δ used in the detailed description, drawings and claims below is a general representation of the optical isomer. ), △ ²⁰ -ginsenoside Rh1, △ ²⁰ -ginsenoside Rh2, △ ²⁰ -ginsenoside PPT was prepared reproducibly to confirm the anticancer effect of this complex ginsenoside, and several single ginsenosides and anticancer Comparing the effect provides a better anticancer composition.

In the present invention, the content of ginsenoside obtained from ginseng or processed ginseng is 85% or more, ginsenoside Rb1 16-23%, ginsenoside Rg1 19-25%, ginsenoside Rd 4-6.3%, ginsenoside Side Re 2-3.8%, Ginsenoside Rg3 5-7.5%, Ginsenoside Rh1 2-3.8%, Ginsenoside Rh2 7-11.5%, Ginsenoside PPT 0.8-1.5, Δ ²⁰ -Ginsenoside Rg3 4 Ginsenoside composition characterized by containing -6.5%, △ ²⁰ -ginsenoside Rh1 1-2.5%, △ ²⁰ -ginsenoside Rh2 6-10%, △ ²⁰ -ginsenoside PPT 0.6-1.3% It is about.
In addition, the present invention has a ginsenoside content of 85% or more obtained from ginseng or processed ginseng, ginsenoside Rb1, ginsenoside Rg1, ginsenoside Rg3, ginsenoside Rh1, ginsenoside Rh2, △ ²⁰ -Ginsenoside Rg3, △ ²⁰ -Ginsenoside Rh1, △ ²⁰ -Ginsenoside Rh2, respectively, characterized in that the ginsenoside composition showing a selective effect on lung cancer. Ginsenoside Rb1, Ginsenoside Rg1, Ginsenoside Rg3, Ginsenoside Rh1, Ginsenoside Rh2, Ginsenoside ΔRg3, Δ ²⁰ -Ginsenoside Rh1 and Δ ²⁰ -Ginsenoside Rh2 are One component in the composition is included in an amount of at least 1% and serves as the main active ingredient.
In addition, the present invention is characterized by additionally containing at least 0.6% or more of each of at least one component of ginsenoside Rd, ginsenoside Re, ginsenoside PPT or ginsenoside △ ²⁰ -ginsenoside PPT, A ginsenoside composition exhibiting a selective effect on lung cancer. Ginsenoside Rd, Ginsenoside Re, Ginsenoside PPT or Ginsenoside Δ ²⁰ -Ginsenoside PPT contains at least 0.6% of one component in the composition of the present invention, and serves as an auxiliary active ingredient.
The present invention also relates to a pharmaceutically acceptable lung cancer selective oral anticancer agent containing the ginsenoside composition (hereinafter referred to as "H-2" or mixed with "H-2") as an active ingredient.

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In addition, the present invention relates to a lung cancer treatment functional food, health supplement or special nutritional products containing the ginsenoside composition as an active ingredient.

Ginsenosides to be used according to the present invention are extracted from the root, leaves, tissue culture of plants such as Panax genus plants containing ginseng saponin, such as Panax ginseng, Panax notojinsaeng, Panax quinquefolium, Panax yaponicus, etc. I can do it.

In addition, the ginsenoside extraction method is capable of extracting each ginsenoside component using an organic solvent layer separation after extraction with hot water or a lower alcohol in a conventional conventional method, as well as using enzymes that are currently developed a lot Conversion and preparation of ginsenoside components are also possible.

A pharmaceutical formulation composition comprising the complex ginsenoside composition of the present invention as an active ingredient or an active ingredient has an effect of strongly inhibiting the growth of lung cancer cells, and thus may be usefully used as an anticancer agent specific to lung cancer. When the ginsenoside composition of the present invention is used clinically as an anticancer agent, it is combined with a carrier commonly used in the pharmaceutical field, and is used for oral administration of a conventional agent in the pharmaceutical field, that is, tablets, capsules, solutions, suspensions, and the like. It is possible to formulate into a variety of preparations, such as preparations, injectable solutions or suspensions, or injectable preparations in the form of ready-to-use injectable dry powders which can be used in the preparation of distilled water for injection.

Carriers that can be used in the pharmaceutical preparations containing the ginsenoside composition of the present invention as an active ingredient are conventional in the pharmaceutical field, for example, in the case of oral preparations, excipients such as starch or sucrose, binders, lubricants , Disintegrants, solubilizers, dispersants, stabilizers, suspending agents and the like, and in the case of injectables, preservatives, analgesic agents, solubilizers, stabilizers and the like can be given. The pharmaceutical preparations thus prepared can be administered orally or parenterally, ie, intravenously, subcutaneously, intraperitoneally. In addition, during oral administration, an antacid may be used in combination or formulated into a coated formulation.

The dosage of the ginsenoside composition of the present invention to the human body may be appropriately selected depending on the absorption rate, inactivation rate and excretion rate of the active ingredient in the body, the age, sex and condition of the patient, the severity of the cancer to be treated, and the like. It is 0.01-100 mg / kg, Preferably it is 0.1-10 mg / kg.

The ginsenoside composition thus formulated may be administered using a specialized dosing method or divided into several times, preferably 1 to 6 times, at regular intervals according to the judgment of the expert and the needs of the individual as needed.

In addition, the present invention includes a complex ginsenoside composition H-2 as an active ingredient, and includes functional foods, dietary supplements or special nutritional supplements for the treatment of lung cancer. As used herein, the term "functional food" means a food product having improved functionality of a general food product by adding the ginsenoside composition to the general food product. In addition, "health supplement" or "special dietary supplement" is a health food prepared by adding the ginsenoside composition H-2 to a general food, or encapsulated-powdered, suspension, etc. It means to bring effect. Unlike general medicine, it has the advantage that there are no side effects that can occur when taking long-term use of the medicine as a raw material.

The content of the functional food, dietary supplements or special nutritional products containing the complex ginsenoside composition of the present invention can be variously changed depending on the food group used, the content is carried out within the toxic range.

Hereinafter, the specific method of the present invention will be described in detail by way of examples. However, the scope of the present invention is not limited only to the description of these examples.

Example 1 Preparation of Complex Ginsenoside H-2

Example 1-1: Separation and Purification of Natural Ginsenosides

1 kg of dried ginseng was extracted with 90% EtOH at 60 for 3 hours and concentrated. This was again performed twice with 90% EtOH at 60 ° C. for 3 hours to obtain about 100 g of the finally obtained extract. This was dissolved in water and passed through a column filled with ion exchange resin (HP-20, Diaion) and adsorbed, followed by desorption with 95% ethanol to obtain 30 g of complex ginsenoside having a purity of 90% or more. Complex ginsenosides were Rb1, Rb2, Rc, Rd, Re, Rg1, and other traces of other ginsenoside mixtures (90% or more of ginsenosides).

<Example 1-2: binary composite from ginsenoside Rg3, △ ²⁰ - Preparation of ginsenoside Rh1 - ginsenoside Rg3, Rh1, △ ^20>

10 g of the complex ginsenoside obtained in Example 1-1 was reacted with 2 L of 50% acetic acid solution (80 ° C., 12 hours). The reactant was passed through a column filled with ion exchange resin (HP-20, Diaion) and adsorbed, followed by desorption with 95% ethanol, Rg3 2.4g, △ ²⁰ -ginsenoside Rg3 2.0g, Rh1 1.7g, and △ A mixture containing 1.7 g of ²⁰ -ginsenoside Rh1 was obtained (purity of the mixture: 85% or more).

Example 1-3 Preparation of F2, F1 Mixtures from Complex Ginsenosides

10 g of the complex ginsenoside obtained in Example 1-1 was reacted with beta-glucosidase derived from Aspergillus or penicillium (55 ° C, 3 days, pH 4) to 1 g of ginsenoside F1 and 4 g of ginsenoside F2. 6 g of a mixture containing was obtained.

<Example 1-4: binary composite from ginsenoside Rh2, △ ²⁰ - prepared ginsenoside mixture PPT - ginsenoside Rh2, PPT, △ ^20>

5 g of the complex ginsenoside obtained in Example 1-3 was reacted with 1 L of 50% acetic acid solution (80 ° C., 12 hours). The reactant was passed through a column filled with ion exchange resin (HP-20, Diaion) and adsorbed, followed by desorption with 95% ethanol. Rh2 2.2g, △ ²⁰ -Ginsenoside Rh2 1.5g, PPT 0.4g, △ ²⁰ A mixture containing 0.3 g of ginsenoside PPT was obtained (purity of the mixture: 85% or more).

Example 1-5 Preparation of Composition H-2

Ginsenoside composition H of the present invention by mixing 3 g of the complex ginsenoside obtained in Example 1-1, 1 g of the complex ginsenoside obtained in Example 1-2 and 1 g of the complex ginsenoside obtained from Example 1-4, respectively. -2 was prepared.

Example 1-6 Component Content of Composite Ginsenoside Composition H-2

The composition of H-2 prepared in Example 1-5 was analyzed by TLC, HPLC and the allowable range of each component of the composition is as follows.

Total ginsenoside content: more than 85%

Rb1 (16-18%), Rg1 (19-20%), Rd (4-5%), Re (2-3%), Rg3 (5-6%), Rh1 (2-3%), Rh2 ( 7-9%), PPT (0.8-1.2), Δ ²⁰ -ginsenoside Rg 3 (4-5%), Δ ²⁰ -ginsenoside Rh 1 (1-2%), Δ ²⁰ -ginsenoside Rh 2 (6 -8%), △ ²⁰ -ginsenoside PPT (0.6-1%)

Example 2: Pharmacological Activity Test

Example 2-1 Anticancer Effect of H-2 Cancer Cells

Skin cancer cells (B16F10, LOX-IMVI), lung cancer cells (NCI-H23), breast cancer cells (MCF7, MDA-MB-231), colon cancer cells (SW620), kidney cancer cells (ACHN), prostate cancer cells (PC-3), Central nerve cancer cells (SNB19) were directly treated with H-2. Treatment concentrations ranged from 0.3 μg / ml to 30 μg / ml, and after treatment for 2 days, the amount of living cells was determined by a sulfohodamine ratio (Sulforhodamin B). The results were expressed as concentrations (GI ₅₀ ) which measured 50% growth inhibition on cancer cells by measuring absorbance (540 nm). The experimental results are shown in Table 2, indicating that H-2 has a cell growth inhibitory effect on skin cancer cells, lung cancer cells, breast cancer cells, colon cancer cells and kidney cancer cells, and central nerve cancer cells.

Example 2-2: Anticancer Effect of H-2 on Lung Cancer Cells (NCI-H23)

Anticancer activity of H-2 against lung cancer cells was verified against NCI-H23 cancer cells. NCI-H23 lung cancer cells were transplanted subcutaneously into nude mice, and H-2 was orally administered once daily at a dose of 3 mg / kg for 33 days after cancer cell transplantation. The size of the cancer cells was measured, and the cancer was isolated and weighed 34 days after cancer cell transplantation.

As shown in Table 3 (anticancer effects on lung cancer cells (NCI-H23) (change in cancer size, mm ³ ), Table 4 (anticancer effects on lung cancer cells (NCI-H23) (cancer weight, mg)), The results of the last day showed that the H-2 treatment group showed a statistically significant inhibitory effect on cancer cell size of 88.5% (p <0.001) compared to the solvent control group, and 86.9% (p <0.001) of the statistically significant tumor weight. A decrease was seen.

These results indicate that the ginsenoside composition H-2 of the present invention has a strong anticancer effect against lung cancer cells (NCI-H23) upon oral administration.

 Experimental group  On day 18  Day 23  Day 27  Day 32  Day 34  Solvent Treatment Group  24.8 ± 13.8  110.7 ± 94.6  149.7 ± 93.9  297.8 ± 101.3  359.9 ± 105.2  H-2 (3 mg / kg)  1.3 ± 1.8 **  5.7 ± 6.4 *  7.3 ± 6.6 **  28.1 ± 21.8 ***  41.2 ± 39.5 ***

* statistically significant at p <0.05 level

** Statistically significant at p <0.01 level

*** Statistically significant at p <0.001 level

 Experimental group  Final dark weight (mg)  Solvent Control  881.2 ± 286.7  H-2 (3 mg / kg)  114.7 ± 71.9 ***

*** Statistically significant at p <0.001 level

Example 2-3 Anticancer Activity of Skin Cancer Cells of H-2

The anticancer activity of H-2 against skin cancer cells was verified against B16F10 cancer cells. B16F10 skin cancer cells were intraperitoneally transplanted with 100,000 cells per BDF1 mouse, and H-2 was administered orally once daily for 15 days after cancer cell transplantation. The death of the animals was observed daily for 30 days.

As shown in Table 5 (anticancer effect on skin cancer cells (B16F10)), there was no effect of prolonging survival of animals by oral treatment of H-2. These results indicate that there is no anticancer effect on skin cancer cells (B16F10) upon oral administration of H-2.

 Experimental group  Average survival rate  ratio  Number of Surviving Animals (30) on Day 30  Solvent Control  19.0 days  100%  0/8  H-2 (3 mg / kg)  19.7 days  100.3%  0/8

Example 2-4 Anticancer Effect of H-2 on Kidney Cancer Cells (ACHN)

Anticancer activity of H-2 against kidney cancer cells was verified against ACHN cancer cells. ACHN kidney cancer cells were implanted subcutaneously into nude mice, and H-2 was administered orally once daily for 26 days after cancer cell transplantation. The size of the cancer cells was measured, and cancer was separated and weighed 27 days after cancer cell transplantation.

As shown in Table 6 (change in cancer size, XIII) and Table 7 (change in cancer weight, mg), there was no decrease in the size and weight of cancer cells by oral treatment of H-2. These results indicate that there is no anticancer effect on kidney cancer cells (ACHN) upon oral administration of H-2.

 Experimental group  Day 10  Day 13  On day 18  Day 23  Day 27  Solvent Control  17.4 ± 8.4  31.6 ± 13.5  54.3 ± 25.6  89.4 ± 42.7  149.3 ± 53.8  H-2 (3 mg / kg)  17.0 ± 7.4  28.1 ± 11.1  51.0 ± 19.1  71.9 ± 30.8  143.0 ± 90.4

 Experimental group  Final dark weight (mg)  Solvent Control  284.4 ± 120.8  H-2 (3 mg / kg)  241.9 ± 241.9

Example 2-5: Anticancer Effect of H-2 on Colon Cancer Cells (SW620)

Anticancer activity of H-2 against colorectal cancer cells was verified against SW620 cancer cells. SW620 colon cancer cells were implanted subcutaneously into nude mice, and H-2 was administered orally once daily for 23 days after cancer cell transplantation. The size of the cancer cells was measured, and cancer was separated and weighed 24 days after cancer cell transplantation.

As shown in Table 8 (change in cancer size, XIII) and Table 9 (change in cancer weight, mg), there was no decrease in the size and weight of cancer cells by oral treatment of H-2. These results indicate that there is no anticancer effect on colon cancer cells (SW620) upon oral administration of H-2.

 Experimental group  Day 11  Day 13  Day 17  Day 22  Day 24 Solvent Control  3.7 ± 3.8  8.5 ± 8.7  36.5 ± 20.8  75.6 ± 48.0  119.5 ± 70.4  H-2 (3 mg / kg)  4.1 ± 4.7  5.6 ± 5.4  38.8 ± 27.4  88.7 ± 64.0  162.7 ± 122.8

 Experimental group  Final dark weight (mg)  Solvent Control  268.7 ± 175.6  H-2 (3 mg / kg)  369.1 ± 331.7

Example 2-6 Anticancer Effect of H-2 on Breast Cancer Cells (MDA-MB-231)

Anticancer activity of H-2 against breast cancer cells was verified against MDA-MB-231 cancer cells. MDA-MB-231 breast cancer cells were implanted subcutaneously into nude mice, and H-2 was administered orally once daily for 14 days after cancer cell transplantation. The size of the cancer cells was measured, and cancer was separated and weighed 15 days after cancer cell transplantation.

As shown in Tables 10 and 11, there was no decrease in the size and weight of cancer cells by oral treatment of H-2. These results indicate that there is no anticancer effect on breast cancer cells (MDA-MB-231) upon oral administration of H-2.

 Experimental group  Day 4  8th day  Day 11  Day 13  Day 15 Solvent Control  32.2 ± 6.9  35.0 ± 4.8  89.7 ± 30.3  163.9 ± 69.6  240.7 ± 109.0  H-2 (3 mg / kg)  28.9 ± 7.0  31.8 ± 5.9  79.3 ± 32.8  170.3 ± 71.1  237.0 ± 96.1

 Experimental group  Final dark weight (mg)  Solvent Control  665.7 ± 297.3  H-2 (3 mg / kg)  658.1 ± 240.4

The present invention is a composition having a high purity ginsenoside mixed composition of more than 85% of a constant component having a selectively superior anticancer effect only to lung cancer. The anti-cancer effect of ginsenosides on lung cancer was analyzed by comparing more than 20 single agents and 10 different ginsenoside combinations, and the complex ginsenoside composition formulation (H-2) of the present invention was Better results were obtained.

The ginsenoside mixed composition of the present invention is meaningful in that it is developed for oral use in the form of a single or combination formulation and developed and provided as a pharmaceutical or food preparation.

In addition, the ginsenoside mixed composition of the present invention is developed for oral administration to remove the inconvenience of the conventionally used injections to help the treatment of lung cancer patients.

In addition, the composition of the composite composition must be constant at all times to exhibit a reproducible pharmacological effect. Unlike the present invention, the present invention provides an opportunity to mass-produce a constant ginsenoside composition to sublimate to the level of a pharmaceutical. have.

Claims (5)

Ginsenoside content of ginseng or processed ginseng is 85% or more, ginsenoside Rb1 16-23%, ginsenoside Rg1 19-25%, ginsenoside Rd 4-6.3%, ginsenoside Re 2 -3.8%, Ginsenoside Rg3 5-7.5%, Ginsenoside Rh1 2-3.8%, Ginsenoside Rh2 7-11.5%, Ginsenoside PPT 0.8-1.5, △ ²⁰ -Ginsenoside Rg3 4-6.5% , Δ ²⁰ -ginsenoside Rh1 1-2.5%, △ ²⁰ -ginsenoside Rh2 6-10%, △ ²⁰ -ginsenoside PPT 0.6-1.3%, ginsenoside for the treatment of lung cancer Composition. Ginsenoside content of ginseng or processed ginseng is 85% or more, ginsenoside Rb1, ginsenoside Rg1, ginsenoside Rg3, ginsenoside Rh1, ginsenoside Rh2, △ ²⁰ -ginsenoside Rg3 ,? ²⁰ -ginsenoside Rh1,? ²⁰ -ginsenoside Rh2, respectively, containing 1% or more and 25% or less, ginsenoside composition for the treatment of lung cancer. 3. The method of claim 2, ginsenoside Rd, ginsenoside Re, ginsenoside PPT or ginsenoside △ ²⁰ - Gene, characterized in that it contains at least one component of the ginsenoside PPT Additionally, each less than 6.3%, more than 0.6% Ginsenoside composition for lung cancer treatment. An oral anticancer agent for treating lung cancer, comprising the composition of any one of claims 1 to 3 as an active ingredient. A dietary supplement for the treatment of lung cancer containing the composition of any one of claims 1 to 3 as an active ingredient.

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