Quinazoline derivative compounds, and uses thereof

Abstract

This invention relates to quinazoline-derived compounds and their medical uses. Specifically, this invention provides compounds capable of treating or preventing c-KIT or PDGFR-related diseases by inhibiting c-KIT or PDGFR.

Description

Quinazoline derivatives and their uses This invention relates to quinazoline-derived compounds and their medical uses. Specifically, this invention relates to compounds capable of treating or preventing c-KIT or PDGFR-related diseases by inhibiting c-KIT or PDGFR. c-KIT is a protein encoding the human KIT gene. The c-KIT receptor is coordinated with stem cell factor (SCF), and an SCF / c-KIT interaction occurs when SCF acts on the c-KIT ligand-binding domain. Consequently, the c-KIT protein dimers and becomes active through autophosphorylation. Activated c-KIT then regulates cell survival, such as growth, differentiation, proliferation, and natural death, through various signal transduction processes, including the intracellular PI3K / Akt system, Ras / MAP kinases, and JAK / STAT. Various cancers associated with c-KIT are related to c-KIT activation. When c-KIT is activated, it can be expressed through ligand interaction, overexpression, or mutation. Overexpression of c-KIT occurs via an autocrine mechanism, and breast cancer, colorectal cancer, small cell lung cancer, and neuroblastoma can occur through this circuit. Furthermore, when gain-of-function mutations occur in c-KIT, regardless of the SCF ligands and their downstream signaling systems, c-KIT becomes resistant to natural death due to overactivation, such as persistent c-KIT activation. Numerous mutations encoding the c-KIT gene have been found in various human cancers, including gastrointestinal stromal tumors (GIST) caused by mutations in the juxtamembranous region of c-KIT, as well as neuroblastoma, acute myeloid leukemia (AML), and systemic mastocytosis (SM) caused by c-KIT mutations. Specifically, the c-KIT D816V mutation (c-KIT D816V), in which the aspartic acid residue at residue 816 of the c-KIT activation circuit is replaced by valine, is predominantly found in mast cell-related diseases, particularly in over 90% of cases meeting the World Health Organization's diagnostic criteria for systemic mastocytosis. Currently, imatinib (Gleevec) and sunitinib (Sutent) have been approved by the FDA for their c-KIT inhibitory activity and for the treatment of GIST patients. They are known to be effective against c-KIT wild-type (c-KIT WT) and c-KIT V560G mutations, but have not been confirmed to inhibit c-KIT D816V. Meanwhile, platelet-derived growth factor receptor (PDGFR) is a tyrosine kinase receptor belonging to the PDGFR family. PDGFR is composed of PDGF-α and PDGF-β subunits, and forms homodimers or heterodimers depending on the binding of growth factors such as PDGF, playing an important role in cell proliferation, cell differentiation, and cell growth and development via intracellular signal transduction. Abnormal signal transduction due to excessive PDGFR activity has been found in a variety of pathological conditions, such as fibrosis, cancer, neurological diseases, and atherosclerosis (Reference [Papadopoulos, Natalia, and Johan Lennartsson. "The PDGF / PDGFR pathway as a drug target." Molecular aspects of medicine 62 (2018): 75-88.]). Systemic sclerosis, a type of fibrotic disease, is a multi-organ disease characterized by fibrosis of the skin and blood vessels, as well as fibrosis of internal organs such as the gastrointestinal tract, lungs, heart, and kidneys. Pulmonary fibrosis, one of the main symptoms of systemic sclerosis, is presumably caused by the uncontrolled proliferation and differentiation of fibroblasts in the lungs into myofibroblasts, and the excessive deposition of extracellular matrix (ECM) proteins in the intercellular space. Thus, there is an increasing unmet need for novel compounds that can be effectively used to treat c-KIT or PDGFR-related diseases by modulating c-KIT or PDGFR activity. [Previous Technical Literature] [Non-Patent Literature] [Papadopoulos, Natalia, and Johan Lennartsson. "The PDGF / PDGFR pathway as a drug target." Molecular aspects of medicine 62 (2018): 75-88.] [Technical Challenge] One objective of this invention is to provide quinazoline-derived compounds, their stereoisomers, or pharmaceutically acceptable salts thereof. Another objective of this invention is to provide a method for preparing the compound. Another objective of the present invention is to provide a compound, particularly a pharmaceutical composition comprising the compound as an active ingredient, for the pharmaceutical use of treating or preventing c-KIT or PDGFR-related diseases, or to provide a method for treating or preventing c-KIT or PDGFR-related diseases, including a method of administering the compound. [Technical Solution] In order to achieve the above objectives, the inventors have made efforts to study and have thus discovered that the following quinazoline derivative compounds represented by Formula 1 inhibit c-KIT or PDGFR activity, and thus completed the present invention. One embodiment of the present invention is a compound represented by the following chemical formula 1, its stereoisomer, or a pharmaceutically acceptable salt thereof. [Chemical Formula 1] In this chemical formula 1, R 1 and R 2 are independently -H, -(C1-C6)alkyl, -(CH 2) m -R X Or -(C=O)-R X {wherein, R 1 and R 2 cannot be methyl at the same time; R X -(C1-C6)alkoxy, -NR A R B -Halogen, cycloalkyl, heterocycloalkyl, aryl, heteroaryl or heterohydroaryl {wherein, at least one H in the cycloalkyl or heterocycloalkyl ring may be via -(C1-C6)alkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)alkyl-O-(C1-C6)alkyl, -(C=O)-(C1-C6)alkyl, -(C=O)-O-(C1-C6)alkyl, -NR C R D , -(=O)-, cycloalkyl or benzyl substitution [wherein, at least one H in the benzyl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)alkoxy, -(C1-C6)haloalkyl or halo]; at least one H in the aryl, heteroaryl or heterohydroaryl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)haloalkyl or halo}; R A and R B Each is independently -H, -(C1-C6)alkyl, cycloalkyl, heterocycloalkyl, aryl, or heteroaryl {wherein at least one H in the cycloalkyl, heterocycloalkyl, aryl, or heteroaryl ring may be substituted with a -(C1-C6)alkyl}; R C and R D Each is independently -H or -(C1-C6)alkyl; m is 0, 1, 2, 3 or 4; R 3 represents -H, -(C1-C6)alkyl, -(C1-C6)alkoxy, or -halogen; L represents -NH(C=O)-L 1-(CH 2) n -L 2-、-NH-S(=O) 2-L 1-(CH 2) n -L 2-、-(C=O)NH-L 1-(CH 2) n -L 2-、-L 1-(CH 2) n -L 2-(C=O)NH- or -NH(C=O)NH-; L 1 and L 2. Each independently constitutes -CR E R F -, -C(=O)NH- or null; R E and R F Each can be independently -H, -(C1-C6)alkyl, or -NH 2. -NH(C=O)O-(C1-C6)alkyl, -OH or -halogen, or R E and R F Combined with carbon to form a -(C3-C6)cycloalkyl; n is 0, 1, 2, 3 or 4; Z is aryl, heteroaryl, heterohydroaryl, cycloalkyl, heterocycloalkyl or -(C2-C6)alkenyl {wherein, at least one H in the aryl, heteroaryl or heterohydroaryl ring may be via -(C1-C6)alkyl, -(C1-C6)haloalkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)cyanoalkyl, -CN, -NR} G R H-(C1-C6)alkoxy or -halo group substitution; at least one H in the cycloalkyl or heterocycloalkyl ring may be substituted with a -(C1-C6)alkyl group; R G and R H Each is independently H or -(C1-C6)alkyl. According to one embodiment of the present invention, compounds represented by the above chemical formula 1, their stereoisomers, or pharmaceutically acceptable salts thereof may include the following categories: R 1 and R 2 are independently -H, -(C1-C6)alkyl, -(CH 2) m -R X Or -(C=O)-R X {wherein, R 1 and R 2 cannot be methyl at the same time; R X -(C1-C6)alkoxy, -NR A R B -Halogen, heterocyclic alkyl, aryl, heteroaryl or heterohydroaryl {wherein, at least one H in the heterocyclic alkyl ring may be via -(C1-C6)alkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)alkyl-O-(C1-C6)alkyl, -(C=O)-(C1-C6)alkyl, -(C=O)-O-(C1-C6)alkyl, -NR C R D , -(=O)-, cycloalkyl or benzyl substitution [wherein, at least one H in the benzyl ring may be substituted by -(C1-C6)alkyl, -(C1-C6)alkoxy, -(C1-C6)haloalkyl or halo]; at least one H in the aryl, heteroaryl or heterohydroaryl ring may be substituted by -(C1-C6)haloalkyl}; R A and R B Each is independently -H, -(C1-C6)alkyl, cycloalkyl, or heteroaryl {wherein at least one H in the cycloalkyl or heteroaryl ring may be substituted with a -(C1-C6)alkyl}; R C and R D Each is independently -H or -(C1-C6)alkyl; m is 0, 1, 2, 3 or 4; R 3 represents -H, -(C1-C6)alkyl, or -halogen; L represents -NH(C=O)-L 1-(CH 2) n -L 2-、-NH-S(=O) 2-L 1-(CH 2) n -L 2-、-(C=O)NH-L 1-(CH 2) n -L 2- or -NH(C=O)NH-; L 1 and L 2. Each independently constitutes -CR E R F - or null; R E and R F Each is independently -H, -(C1-C6)alkyl or -NH 2, or R E and R F It combines with carbon to form a -(C3-C6)cycloalkyl group; n is 0, 1, 2, 3 or 4; Z is phenyl, 5-10-membered heteroaryl, 5-10-membered heterohydroaryl, 5-10-membered heterocycloalkyl or -(C2-C6)alkenyl {wherein, at least one H in the phenyl, the 5-10-membered heteroaryl or the 5-10-membered heterohydroaryl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)haloalkyl, -CN, -(C1-C6)alkoxy or -halo; at least one H in the 5-10-membered heterocycloalkyl ring may be substituted with -(C1-C6)alkyl}. According to one embodiment of the present invention, compounds represented by the above chemical formula 1, their stereoisomers, or pharmaceutically acceptable salts thereof may include the following categories: R 1 and R 2 are independently -H, -(C1-C6)alkyl, -(CH 2) m -R X Or -(C=O)-R X {wherein, R 1 and R 2 cannot be methyl at the same time; R X -(C1-C6)alkoxy, -NR A R B -Halogen, heterocyclic alkyl, aryl, heteroaryl or heterohydroaryl {wherein, the heterocyclic alkyl is monocyclic, spirocyclic, bridged ring or fused ring, and at least one H in the heterocyclic alkyl ring may be via -(C1-C6)alkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)alkyl-O-(C1-C6)alkyl, -(C=O)-(C1-C6)alkyl, -(C=O)-O-(C1-C6)alkyl, -NR C R D , -(=O)-, cycloalkyl or benzyl substitution [wherein, at least one H in the benzyl ring may be substituted by -(C1-C6)alkyl, -(C1-C6)alkoxy, -(C1-C6)haloalkyl or halo]; at least one H in the aryl, heteroaryl or heterohydroaryl ring may be substituted by -(C1-C6)haloalkyl}; R A and R B Each is independently -H, -(C1-C6)alkyl, cycloalkyl, or heteroaryl {wherein at least one H in the cycloalkyl or heteroaryl ring may be substituted with a -(C1-C6)alkyl}; R C and R D Each is independently -H or -(C1-C6)alkyl; m is 0, 1, 2 or 3. According to one embodiment of the present invention, compounds represented by Chemical Formula 1 above, their stereoisomers, or pharmaceutically acceptable salts thereof may include the following categories: compounds represented by Chemical Formula 1 are represented by Chemical Formula 2; [Chemical Formula 2] In this chemical formula 2, R 3 can be -H, -(C1-C6)alkyl, or -halogen. According to one embodiment of the present invention, the compound represented by the above chemical formula 1, its stereoisomers, or its pharmaceutically acceptable salts may include the following categories: L is -NH(C=O)-L 1-(CH 2) n -L 2-、-NH-S(=O) 2-L 1-(CH 2) n -L 2-、-(C=O)NH-L 1-(CH 2) n -L 2- or -NH(C=O)NH-; L 1 and L 2. Each independently constitutes -CR E R F - or null; R E and R F Each is independently -H, -(C1-C6)alkyl or -NH 2, or R E and R F It combines with carbon to form -(C3-C6)cycloalkyl groups; n is 0, 1, 2 or 3. According to one embodiment of the present invention, the compound represented by the above chemical formula 1, its stereoisomers or its pharmaceutically acceptable salts may include the following categories: Z is phenyl, 5-10-membered heteroaryl, 5-10-membered heterohydroaryl, 5-10-membered heterocyclic alkyl or -(C2-C6)alkenyl {wherein, at least one H in the phenyl, the 5-10-membered heteroaryl or the 5-10-membered heterohydroaryl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)haloalkyl, -CN, -(C1-C6)alkoxy or -halo; at least one H in the 5-10-membered heterocyclic alkyl ring may be substituted with -(C1-C6)alkyl}. In addition, according to a specific embodiment of the present invention, the compound represented by chemical formula 1 may be selected from the group of compounds of Examples 1 to 169 listed in Tables 1 to 5 below. One embodiment of the present invention is a pharmaceutical composition comprising a compound represented by chemical formula 1, its stereoisomer or a pharmaceutically acceptable salt thereof as an active ingredient. In this invention, unless otherwise specified, "alkyl" may refer to a straight-chain or branched non-cyclic group, a cyclic group, or a combination thereof in a saturated hydrocarbon. For example, "C 1 - "6-alkyl" can indicate an alkyl group containing 1 to 6 carbon atoms. Acyclic alkyl groups can include, for example, methyl, ethyl, n-propyl, n-butyl, isopropyl, secondary butyl, isobutyl, tertiary butyl, and similar groups, but are not limited thereto. Cyclic alkyl groups are used interchangeably with "cycloalkyl" as used herein, and for example can include cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, cyclooctyl, and similar groups, but are not limited thereto. In this invention, "alkoxy" can indicate that -(O-alkyl) is an alkyl ether group, wherein the alkyl group is the same as defined above. For example, "C 1 - "6-alkoxy" can mean that it contains C 1 - 6-alkyl alkoxy group, i.e. -(OC 1 - (6 alkyl), and for example, alkoxy groups may include, but are not limited to, methoxy, ethoxy, n-propoxy, isopropoxy, n-butoxy, isobutoxy, secondary butoxy, tertiary butoxy and similar groups. In this invention, the "halogen group" can be F, Cl, Br or I. In this invention, "haloalkyl" can mean a straight-chain or branched alkyl (hydrocarbon) having one or more halocarbon atoms as defined herein. Examples of haloalkyl may include, but are not limited to, methyl, ethyl, propyl, isopropyl, isobutyl, or n-butyl that are independently substituted with one or more halogens, such as F, Cl, Br, or I. In this invention, "hydroxyalkyl" can mean a straight-chain or branched-chain alkyl (hydrocarbon) having carbon atoms substituted with hydroxyl (OH). In this invention, "aminoalkyl" can mean a straight-chain or branched-chain alkyl (hydrocarbon) (NR'R") having a carbon atom substituted with an amino group. Here, R' and R" can each be independently selected from hydrogen and C. 1 - The group of 6 alkyl groups, wherein the selected R' and R" may be substituted or unsubstituted independently. In this invention, "cyanoalkyl" can mean a straight-chain or branched-chain alkyl (hydrocarbon) having carbon atoms substituted with cyano (CN). In this invention, "heterocyclic alkyl" can mean a ring containing at least one of N, O, P, P(=O), and S, and can be saturated or partially unsaturated. Here, when unsaturated, it can be called a heterocyclic alkene. Unless otherwise stated, heterocyclic alkyl can be monocyclic or polycyclic, such as spirocyclic, bridged, or fused rings. Additionally, "3 to 12-membered heterocyclic alkyl" can mean a heterocyclic alkyl containing 3 to 12 atoms forming the ring, and for example, heterocyclic alkyl can include pyrrolidine, piperidine, imidazoidine, pyrazolidine, butyrolactamine, valproic acid, imidazolidinone, hydantoin, m-dioxane, phthalimide, piperidine, pyrimidine-2,4(1 H,3 H)-Diketone, 1,4-dimethyl methacrylate, morpholine, thiomorpholine, thiomorpholine- S-oxide, thiomorpholine- S, S-oxides, piperan, piperan, pyridone, 3-pyrroline, thiopiperan, pyron, tetrahydrofuran, tetrahydrothiophene, quinine ring, tropane, 2-azaspiro[3.3]heptane, (1 R,5 S)-3-azabicyclo[3.2.1]octane, (1 s,4 s)-2-azabicyclo[2.2.2]octane, (1 R,4 R)-2-oxa-5-azabicyclo[2.2.2]octane and similar groups, but not limited thereto. In this invention, "aromatic hydrocarbon" can mean an aromatic hydrocarbon ring. Aromatic hydrocarbons can be monocyclic or polycyclic aromatic hydrocarbons. The number of carbon atoms in the ring of an aromatic hydrocarbon can be 5 or more and 30 or less, 5 or more and 20 or less, or 5 or more and 15 or less. Examples of aromatic hydrocarbons may include, but are not limited to, benzene, naphthalene, fluorene, anthracene, phenanthrene, biphenyl, terphenyl, tetraphenyl, pentphenyl, hexaphenyl, terphenyl, pyrene, benzopropadiene, β- and similar groups. In this specification, a residue obtained by removing a hydrogen atom from the above "aromatic hydrocarbon" is called an "aryl". In this invention, "heteroaromatic hydrocarbon" can be a ring containing one or more of the heteroelements O, N, P, Si, and S. The number of carbon atoms in the ring of a heteroaromatic hydrocarbon can be 2 or more and 30 or less, or 2 or more and 20 or less. Heteroaromatic hydrocarbons can be monocyclic or polycyclic. Polycyclic heteroaromatic hydrocarbons can have, for example, bicyclic or tricyclic structures. Examples of heteroaromatic hydrocarbons may include thiophene, purine, pyrrole, pyrazole, imidazole, thiazole, acetazole, isothiazole, acediazole, triazole, pyridine, dipyridyl, triazine, acridine, pyridyl, quinoline, quinazoline, quinazonium, phenoxazine, pyridine, pyridopyrimidine, pyridopyrimidine, pyridopyrimidine, isoquinoline, indole, carbazole, imidazodopyridyl, imidazopyridine, imidazopyrimidine, pyrazopyrimidine, imidazopyrimidine, pyrazopyrimidine, imidazopyrimidine, pyrazopyridine. N-arylcarbazole, N-Heteroarylcarbazole, N-alkylcarbazole, benzo[a]azole, benzimidazole, benzo[thiazolium]azole, benzo[a]carbazole, benzo[thiaphene], dibenzo[thiaphene], thiophene[thiaphene], benzo[furan], phenophylline, isobenzoazole, acediazole, thiadiazole, benzo[thiazolium]azole, tetrazolium, phenophylline, dibenzosilol, dibenzofuran, and similar groups, but not limited thereto. In one embodiment of the invention, heteroaromatic hydrocarbons may also include bicyclic heterocyclic aromatic hydrocarbons containing an aromatic ring fused to a heterocyclic alkyl ring or a heteroaromatic hydrocarbon fused to a cycloalkyl ring. In this specification, a residue obtained by removing a hydrogen atom from a "heteroaromatic hydrocarbon" is called a "heteroaryl". In this invention, "hydroaromatic" or "hydroaryl" means that one or more double bonds in an aromatic hydrocarbon ring are saturated. In this invention, "heterohydroaromatic" or "heterohydroaryl" means that one or more double bonds in the "heteroaromatic" or "heteroaryl" ring are saturated. In this invention, "ring" can be monocyclic or polycyclic. Polycyclic rings can be spirocyclic, bridged rings, or fused rings. In this invention, the term "stereoisomer" means that the compounds or their salts have the same chemical formula or molecular formula but are spatially different. Each of these stereoisomers and mixtures thereof are also included within the scope of this invention. Unless otherwise stated, solid lines bonded to asymmetric carbon atoms (…) ) may include wedge-shaped solid line keys ( ) or wedge-shaped dashed key ( ), which represents the absolute arrangement of the center of a three-dimensional structure. The compound of Formula 1 of this invention can exist in the form of a "medically acceptable salt". As a salt, an acid addition salt formed from a pharmaceutically acceptable free acid is useful. The term "medically acceptable salt" refers to any organic or inorganic acid addition salt of the compound, whose side effects do not diminish the beneficial efficacy of the compound represented by Formula 1 at concentrations where it is effective, and which is relatively non-toxic and harmless to the patient. Acid addition salts are prepared by conventional methods, such as by dissolving the compound in an excess of an aqueous acid solution and precipitating the salt using a water-miscible organic solvent, such as methanol, ethanol, acetone, or acetonitrile. An equal molar amount of the compound and an aqueous solution of the acid or alcohol can be heated, and the mixture can then be evaporated to dryness, or the precipitated salt can be filtered out by suction. Here, organic and inorganic acids can be used as free acids, wherein the inorganic acid can be hydrochloric acid, phosphoric acid, sulfuric acid, nitric acid or similar acids, and the organic acid can be methanesulfonic acid, p-toluenesulfonic acid, acetic acid, trifluoroacetic acid, maleic acid, succinic acid, oxalic acid, benzoic acid, tartaric acid, fumaric acid, mandelic acid, propionic acid, citric acid, lactic acid, glycolic acid, gluconic acid, galacturonic acid, glutamic acid, glutaric acid, glucuronic acid, aspartic acid, ascorbic acid, carbonic acid, vanillic acid, hydroiodic acid or similar acids. However, it is not limited to these. Additionally, pharmaceutically acceptable metal salts can be prepared using alkalis. For example, by dissolving the compound in an excess solution of an alkali metal hydroxide or alkaline earth metal hydroxide, filtering the undissolved salt, and subsequently evaporating and drying the filtrate, an alkali metal salt or alkaline earth metal salt can be obtained. Sodium, potassium, or calcium salts are particularly suitable for preparation here, but not limited to these. Furthermore, corresponding silver salts can be obtained by reacting an alkali metal or alkaline earth metal salt with a suitable silver salt (e.g., silver nitrate). Unless otherwise specified, pharmaceutically acceptable salts of this invention include salts of acidic or basic groups that may be present in compounds of Formula 1. For example, pharmaceutically acceptable salts may include sodium, calcium, and potassium salts of hydroxyl groups, and other pharmaceutically acceptable salts of amino groups may include hydrobromide, sulfate, hydrogen sulfate, phosphate, hydrogen phosphate, dihydrogen phosphate, acetate, succinate, citrate, tartrate, lactate, amygdalinate, methanesulfonate (methanesulfonate), and p-toluenesulfonate (toluenesulfonate) and similar salts; and may be prepared by methods of salt preparation known in this art. The use of quinazoline-derived compounds: One embodiment of the present invention is a composition for inhibiting c-KIT or PDGFR, comprising a compound represented by the following chemical formula 1, its stereoisomer, or a pharmaceutically acceptable salt thereof as an active ingredient. Another embodiment of the present invention is a pharmaceutical composition comprising this compound for treating or preventing c-KIT or PDGFR-related diseases. [Chemical Formula 1] Chemical formula 1 is as defined above. According to one embodiment of the present invention, the quinazoline derivative represented by Formula 1 exhibits excellent inhibitory activity against c-KIT or PDGFR, and is therefore used to treat or prevent c-KIT or PDGFR-related diseases. In this invention, c-KIT-related diseases may be selected from one or more of cancer or mast cell-related diseases, but are not limited thereto. In this invention, among c-KIT-related diseases, cancer may be any one or more of the following groups: leukemia, skin cancer, breast cancer, rectal cancer, lung cancer, neuroblastoma, thyroid cancer, germ cell tumor, prostate cancer, and gastrointestinal stromal tumor, but is not limited thereto. In this invention, among c-KIT-related diseases, mast cell-related diseases may include mastocytosis, acne, progressive ossifying fibrosis and cystic fibrosis; acute nephrotic syndrome, glomerulonephritis, renal amyloidosis, renal interstitial fibrosis and inflammatory myopathy; HIV, type II diabetes, cerebral ischemia, CNS diseases, bacterial infections, interstitial cystitis and inflammatory bowel disease; tumor angiogenesis; autoimmune diseases and allergic diseases, or one or more of these, but are not limited thereto. Meanwhile, in this invention, PDGFR-related diseases may be selected from one or more of fibrosis, cancer, neurological diseases, atherosclerosis, and pulmonary hypertension, but are not limited thereto. In this invention, fibrosis in PDGFR-related diseases includes all fibrosis that can be attributed to the inhibition of PDGFR activity and thus exhibit preventive or therapeutic effects, and specifically, it may be selected from any one or more of the following: systemic sclerosis, pulmonary fibrosis, liver fibrosis, cirrhosis, renal fibrosis, myelofibrosis, myocardial fibrosis, sarcomatoid disease, keloid, burn-induced hypertrophic scar, proliferative retinopathy, glaucoma, cataract, posterior capsular opacification, angioplasty, restenosis following vascular surgery or vascular injury, cystic fibrosis, and Marfan syndrome, but is not limited thereto. In this invention, cancer in PDGFR-related diseases includes all cancers that can be attributed to the inhibition of PDGFR activity and exhibit preventive or therapeutic effects, and can be solid cancers or hematologic malignancies. For example, cancer can be any one or more of the following groups: squamous cell carcinoma, small cell lung cancer, non-small cell lung cancer, lung adenocarcinoma, lung squamous cell carcinoma, peritoneal cancer, skin cancer, skin or ocular melanoma, rectal cancer, perianal adenocarcinoma, esophageal cancer, small bowel cancer, endocrine gland cancer, parathyroid cancer, adrenal cancer, soft tissue sarcoma, urethral cancer, chronic or acute leukemia, lymphocytic lymphoma, hepatocellular carcinoma, gastrointestinal cancer, gastric cancer, pancreatic cancer, glioblastoma, cervical cancer, ovarian cancer, liver cancer, bladder cancer, liver tumor, breast cancer, colon cancer, colorectal cancer, endometrial cancer or uterine cancer, salivary gland cancer, kidney cancer, prostate cancer, vulvar cancer, thyroid cancer, head and neck cancer, brain cancer, osteosarcoma, but is not limited thereto. Cancer includes not only primary cancer but also metastatic cancer. In this invention, among PDGFR-related diseases, neurological diseases include all neurological diseases that can be attributed to the inhibition of PDGFR activity and thus present a preventive or therapeutic effect, and specifically, they may be selected from any one or more of the following: central nervous system diseases, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, multiple sclerosis, Huntington's disease, Alzheimer's disease, epilepsy, amyotrophic lateral sclerosis, stroke and brain or spinal cord injury followed by nerve damage and axonal degeneration-related conditions, but are not limited thereto. In this invention, atherosclerosis, among PDGFR-related diseases, includes all atherosclerosis that can be attributed to the prevention or treatment of PDGFR activity. In this invention, among PDGFR-related diseases, pulmonary hypertension includes all pulmonary hypertension that can be attributed to the inhibition of PDGFR activity and thus present a preventive or therapeutic effect. In addition to the compound represented by Formula 1, its stereoisomers, or its pharmaceutically acceptable salts, the pharmaceutical compositions of the present invention may further include one or more pharmaceutically acceptable carriers for administration. Pharmaceutically acceptable carriers may be physiological saline, sterile water, Ringer's solution, buffered physiological saline, dextran solution, maltodextrin solution, glycerol, ethanol, and mixtures of one or more of these components, and other known additives, such as antioxidants, buffers, and antibacterial agents, may be added as needed. Furthermore, diluents, dispersants, surfactants, binders, and lubricants may be added to prepare formulations for injection, such as aqueous solutions, suspensions, emulsions, pills, capsules, granules, or tablets. Therefore, the compositions of the present invention may be patches, liquids, pills, capsules, granules, tablets, suppositories, or the like. These formulations can be prepared using conventional methods of formulation in this technology or methods disclosed in the literature [Remington's Pharmaceutical Science, Mack Publishing Company, Easton PA], and can be formulated into various formulations depending on the disease or ingredient. In addition to the compound represented by Formula 1, its stereoisomers, or its pharmaceutically acceptable salts, the pharmaceutical compositions of the present invention may further include one or more active ingredients exhibiting the same or similar efficacy. The pharmaceutical compositions of the present invention can be used for clinical administration and can be prepared for administration in various oral and non-enteral dosage forms. This invention provides a method for preventing or treating c-KIT or PDGFR-related diseases, comprising: administering to an individual in need a therapeutically effective amount of a compound represented by Formula 1, its stereoisomer, or a pharmaceutically acceptable salt thereof. The individual may be a mammal, including a human. The term "therapeutic effective amount" as used in this invention refers to the amount of a compound represented by Chemical Formula 1 that is effective in preventing or treating c-KIT or PDGFR-related diseases. Specifically, "therapeutic effective amount" means an amount sufficient to treat the disease with a reasonable benefit / risk ratio suitable for medical treatment, and the effective dose level can be determined by factors including individual type and severity, age, sex, disease type, drug activity, drug sensitivity, time of administration, route of administration and elimination rate, duration of treatment, factors including concurrently used drugs, and other factors well known in the medical field. The pharmaceutical compositions of this invention can be administered as individual therapeutic agents or in combination with other therapeutic agents, and can be administered sequentially or simultaneously with commercially available therapeutic agents. Furthermore, the pharmaceutical compositions of this invention can be administered as a single dose or multiple doses. Importantly, the minimum amount that achieves maximum effect without side effects, taking into account all the above factors, can be easily determined by those skilled in the art. The dosage of the pharmaceutical compositions of this invention can be determined by experts based on various factors such as the patient's condition, age, sex, complications, and similar factors. Because the active ingredient of the pharmaceutical composition of the present invention has excellent safety, it can be used in addition to the determined dosage. Furthermore, the present invention can inhibit c-KIT or PDGFR by administering to mammals, including humans, a compound represented by chemical formula 1, its stereoisomer, or a pharmaceutically acceptable salt thereof. Furthermore, according to one embodiment of the present invention, the present invention provides the use of a compound represented by Chemical Formula 1, its stereoisomers, or a pharmaceutically acceptable salt thereof for the preparation of a medicament for the treatment of c-KIT or PDGFR-related diseases. The compound represented by Chemical Formula 1 used in the preparation of the medicament can be mixed with acceptable adjuvants, diluents, carriers, and the like, and can be prepared into a combination formulation with other active agents to achieve a synergistic effect of the active ingredient. One embodiment of the present invention provides a method for treating or preventing any or more diseases selected from the group consisting of: cancer, mast cell-related diseases, fibrotic diseases, neurological diseases, atherosclerosis, and pulmonary hypertension, the method comprising administering to an individual in need a therapeutically effective amount of a compound represented by chemical formula 1, its stereoisomer, or a pharmaceutically acceptable salt thereof. One embodiment of the present invention provides a method for inhibiting c-KIT or PDGFR, the method comprising administering to an individual in need a therapeutically effective amount of a compound represented by chemical formula 1, its stereoisomer, or a pharmaceutically acceptable salt thereof. One embodiment of the present invention provides the use of a compound represented by chemical formula 1, its stereoisomers or a pharmaceutically acceptable salt thereof, for the preparation of an agent for the treatment or prevention of any or more diseases selected from the group consisting of: cancer, mast cell-related diseases, fibrotic diseases, neurological diseases, atherosclerosis and pulmonary hypertension. One embodiment of the present invention provides the use of a compound represented by chemical formula 1, its stereoisomers or a pharmaceutically acceptable salt thereof, for the preparation of a medicament for the treatment or prevention of c-KIT or PDGFR-related diseases. Unless they contradict each other, the contents mentioned in the uses, compositions, treatment methods and the like of this invention also apply. This research was supported by the Korea Drug Development Fund (RS-2022-00165937, Republic of Korea), funded by the Ministry of Science and ICT, the Ministry of Trade, Industry and Energy, and the Ministry of Health and Welfare. [Advantageous Effects] The novel compounds of this invention exhibit an inhibitory effect on c-KIT or PDGFR activity. Therefore, the compounds of this invention can be effectively used to treat or prevent c-KIT or PDGFR-related diseases. The components and functions of the present invention will be described in more detail below by way of examples. However, the examples presented below are merely illustrative and the scope of the invention is not limited thereto. Since commercially available reagents are readily available without further purification, they are used. In this invention, room temperature refers to a temperature between 20°C and 25°C, and a rotary evaporator is used for concentration under reduced pressure or solvent removal by distillation. < Methods and conditions for analysis and purification > In this invention, a series of compounds synthesized by example are synthesized, purified by the following methods, and their structures are analyzed. 1. The analytical conditions for the compound were as follows: High-performance liquid chromatography (HPLC) was performed using a Waters UPLC system equipped with a mass QDa detector (ACQUITY UPLC PDA detector). The column used for compound purification was a Waters ACQUITY UPLC BEH C18 (1.7 μm, 2.1 × 50 mm), and the column temperature was set at 30°C. Water containing 0.1% formic acid was used as mobile phase A, and acetonitrile containing 0.1% formic acid was used as mobile phase B. The gradient conditions were 10-100% B over 3 minutes, and the flow rate was 0.6 mL / min. In this specification, HPLC and UPLC are used as interchangeable terms. 2. Purification conditions of the compound (1) Medium-pressure liquid chromatography (MPLC) for purification Medium-pressure liquid chromatography was performed using a TELEDYNE ISCO CombiFlash Rf+UV ​​(60 min). (2) Preparative HPLC 1) Preparative liquid chromatography-mass spectrometry (preparative LCMS) for purification The compound was purified using a Waters automated purification HPLC system equipped with a mass QDa detector (2767 sample manager, 2545 binary gradient module, 2998 photodiode array detector). The column used was a Waters SunFire preparative C18 OBDTM (5 μm, 19 × 50 mm), and the column temperature was maintained at room temperature. Water containing 0.035% trifluoroacetic acid was used as mobile phase A, and methanol containing 0.035% trifluoroacetic acid was used as mobile phase B. The gradient conditions were 15-100% B over 10 min, and the flow rate was 25 mL / min. 2) Compounds were purified using a preparative 150 LC system (preparative liquid chromatography with UV spectroscopy) with a Waters preparative 150 LC system (2545 quadruple gradient module, 2998 photodiode array detector, and dissolution collector III). The column used was a Waters XTerra preparative RP18 OBDTM (10 μm, 30 × 300 mm), and the column temperature was maintained at room temperature. 3) Compounds were purified using an ACCQ preparative HP150 system with a Teledyne Isco ACCQ preparative HP150 system. The column used was a Waters XTerra preparative RP18 OBDTM (10 μm, 30 × 300 mm), and the column temperature was maintained at room temperature. 3. NMR NMR spectra were analyzed using a Bruker AVANCE III 400 or AVANCE III 400 HD instrument, and the data were expressed in parts per million (ppm, δ). Preparation examples are shown below. Although salts (e.g., TFA, HCl) are used in the actual preparation methods, they may not be included in the reaction flow of each preparation example. < Example 1> N -( 4 -( 7 -( 2 -( Diethylamino ) ethoxy )- 6 - Methoxyquinazoline - 4 - base ) Phenyl )- 2 -( 4 -( Trifluoromethyl ) Phenyl ) Preparation of acetamide Step 1: Under nitrogen atmosphere, 4-aminophenylboronic acid pinacol ester hydrochloride (0.50 g, 2.88 mmol), 7-(benzyloxy)-4-chloro-6-methoxyquinazoline (0.87 g, 2.88 mmol), tetrakis(triphenylphosphine)palladium(0) (0.30 g, 0.87 mmol), and sodium carbonate (0.61 g, 5.77 mmol) were dissolved in 1,4-dimethylamine (11.1 ml) and distilled water (3.3 ml), followed by oxygen removal for 10 minutes. After reacting the reaction mixture at 80°C for 3 hours, distilled water was added to the reaction mixture, and the organic matter was subsequently extracted with ethyl acetate (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the mixture was concentrated under reduced pressure. The concentrated organic layer was crystallized from dichloromethane and subsequently filtered to give the desired compound, 4-(7-(benzylmethyloxy)-6-methoxyquinazoline-4-yl)aniline (0.80 g, 78%). MS (m / z): 358.3 [M+H] + UPLC rt (min): 1.37 Step 2: Dissolve 2-(4-(trifluoromethyl)phenyl)acetic acid (1.62 g, 7.93 mmol) and 1-[bis(dimethylamino)methylene]-1H-1,2,3-triazolo[4,5,-b]pyridinium 3-oxide hexafluorophosphate (HATU) (4.02 g, 10.58 mmol) in dimethylformamide (13.2 ml), then add dropwise. N, N-Diisopropylethylamine (2.73 g, 21.15 mmol). 4-(7-(benzylmethyloxy)-6-methoxyquinazoline-4-yl)aniline (2.70 g, 5.29 mmol), obtained in step 1, was added dropwise to the reaction mixture, followed by stirring at room temperature for 3 hours. After adding distilled water to the reactants, the organic matter was extracted with ethyl acetate (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the mixture was concentrated under reduced pressure. The concentrated mixture was purified by MPLC (EtOAc:Hex = 10-100%) to give the desired compound as a solid. N-(4-(7-(benzylmethyloxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (2.30 g, 80%). MS (m / z): 544.3 [M+H] + UPLC rt(min): 1.83 Step 3: Obtain the information from Step 2 N-(4-(7-(benzyloxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (1.20 g, 2.21 mmol) was dissolved in methanol (11.0 ml), and then Pd / C (0.20 g, 0.44 mmol) was added. The reaction mixture was stirred at 25 °C under hydrogen atmosphere for 1 hour. The reactants were filtered through a diatomaceous earth filter, washed with methanol, and then concentrated under reduced pressure. After concentration, it was purified by MPLC (DCM:MeOH = 0-10%) to give the desired compound. N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.78 g, 78%). MS (m / z): 454.1 [M+H] + UPLC rt(min): 1.47 Step 4: Obtain the information from Step 3 N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.09 g, 0.20 mmol), 2-chloro- N, N-Diethylethane-1-amine hydrochloride (0.04 g, 0.24 mmol) and potassium carbonate (0.05 g, 0.40 mmol) were dissolved in dimethylformamide (2.0 ml), and then added dropwise. N, N-Diisopropylethylamine (0.05 g, 0.40 mmol) was reacted and stirred at 90 °C for 6 hours. After confirming the reaction was complete and distilled water was added, the organic matter was extracted with ethyl acetate (×3). The collected organic layer was washed with brine, and the remaining water was removed with sodium sulfate and concentrated under reduced pressure. After concentration, it was purified by MPLC (DCM:MeOH=0-10%) to obtain the desired compound. N-(4-(7-(2-(diethylamino)ethoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.05 g, 45.6%). MS (m / z): 553.4 [M+H] + UPLC rt(min): 1.35 < Example 2> N -( 4 -( 6 - methoxy - 7 -(( 1 - Methylpiperidine - 4 - base ) Oxygen ) Quinazoline - 4 - base ) Phenyl )- 2 -( 4 -( Trifluoromethyl ) Phenyl ) Preparation of acetamide Step 1: Obtain the information from Step 3 of Example 1 N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.05 g, 0.11 mmol), 1-methylpiperidin-4-ol (0.02 g, 0.17 mmol), and triphenylphosphine (0.09 g, 0.33 mmol) were dissolved in dichloromethane (1.1 ml), followed by dropwise addition of diisopropyl azodicarbonate (0.07 g, 0.33 mmol). After stirring overnight at room temperature, the reaction was concentrated under reduced pressure and purified by MPLC (DCM:MeOH=0-10%) to obtain the desired compound. N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)oxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.02 g, 33%). MS (m / z): 551.3 [M+H] + UPLC rt(min): 1.32 < Example 3> N -( 4 -( 6 - methoxy - 7 -( 2 -( 4 - Methylpiperazine 𠯤 - 1 - base ) ethoxy ) Quinazoline - 4 - base ) Phenyl )- 2 -( 4 -( Trifluoromethyl ) Phenyl ) Preparation of acetamide Step 1: Obtain the information from Step 3 of Example 1 N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (80.0 mg, 0.18 mmol), 2-bromoethanol (35.3 mg, 0.28 mmol), and triphenylphosphine (64.8 mg, 0.25 mmol) were dissolved in dichloromethane (1.7 ml), followed by dropwise addition of diisopropyl azodicarbonate (42.8 mg, 0.21 mmol), and the mixture was stirred overnight at room temperature. Upon completion of the reaction, the mixture was concentrated under reduced pressure and purified by MPLC (EtOAc:Hex = 30-100%) to obtain the desired compound. N-(4-(7-(2-bromoethoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (80.0 mg, 81%). MS (m / z): 562.1 [M+H] + UPLC rt(min): 1.71 Step 2: Obtain the information from Step 1 N-(4-(7-(2-bromoethoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.05 g, 0.09 mmol) and 1-methylpiperazine (0.04 g, 0.36 mmol) were dissolved in dimethylformamide (0.9 ml), and then added dropwise. N, N-Diisopropylethylamine (0.02 g, 0.18 mmol) was added and then stirred overnight at room temperature. After the reaction was complete, distilled water was added, and the organic matter was extracted with ethyl acetate (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the mixture was concentrated under reduced pressure. The concentrated mixture was purified by MPLC (EtOAc:Hex = 30-100%) to obtain the desired compound. N-(4-(6-methoxy-7-(2-(4-methylpiperazolin-1-yl)ethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (11.0 mg, 65.5%). MS (m / z): 580.4 [M+H] + UPLC rt(min): 1.26 < Example 4> N -( 4 -( 7 -(( 1 - Ethylpiperidine - 4 - base ) methoxy )- 6 - Methoxyquinazoline - 4 - base ) Phenyl )- 2 -( 4 -( Trifluoromethyl ) Phenyl ) Preparation of acetylamine Step 1: Take the result obtained in step 3 of Example 1. N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.10 g, 0.22 mmol) and tributyl 4-((toluenesulfonyloxy)methyl)piperidine-1-carboxylate (0.12 g, 0.33 mmol) were dissolved in dimethylformamide (1.1 ml), followed by dropwise addition of potassium carbonate (0.06 g, 0.44 mmol). The reaction mixture was stirred overnight at 70 °C. Upon completion of the reaction, the desired compound, 4-(((6-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamide)phenyl)quinazoline-7-yl)oxy)methyl)piperidine-1-carboxylate (0.08 g, 55.7%), was purified by MPLC (DMC:MeOH = 0-10%). MS (m / z): 651.4 [M+H] + UPLC rt(min): 1.99 Step 2: The tributyl 4-(((6-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetaminophen)phenyl)quinazolin-7-yl)oxy)methyl)piperidin-1-carboxylic acid obtained in Step 1 (0.08 g, 0.12 mmol) was dissolved in dichloromethane (1.2 ml), and then trifluoroacetic acid (0.14 g, 1.229 mmol) was slowly added dropwise at 0 °C. After stirring the reaction mixture overnight at room temperature, it was concentrated and purified by preparative HPLC to give the desired compound N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetaminophen 2,2,2-trifluoroacetate (7.5 mg, 92%). MS (m / z): 551.3 [M+H] + UPLC rt(min): 1.40 Step 3: Dissolve the N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide 2,2,2-trifluoroacetate (0.03 g, 0.05 mmol), sodium triacetoxyborohydride (0.02 g, 0.09 mmol), and acetaldehyde (2.98 mg, 0.07 mmol) obtained in Step 2 in 1,4-dimethylamine (0.5 ml), and then add the following dropwise: N, N-Diisopropylethylamine (0.03 g, 0.23 mmol). After stirring the reaction mixture overnight at room temperature, the desired compound was obtained by preparative HPLC purification upon completion. N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.01 g, 38%). MS (m / z): 595.4 [M+H] + UPLC rt(min): 1.50 Example 1 to Examples 5 to 54 were prepared in a manner similar to that of Examples 1 to 4, and the compound names, NMR, mass and UPLC analysis results of Examples 1 to 54 are summarized in Table 1 below. In the above preparation examples, even though the compounds were prepared in salt form, they are listed in free form in the table. Therefore, the salt actually used in the preparation method can be added to the compound without added salt, or other salts can be added. [Table 1] < Example 55> N -( 4 -( 6 - methoxy - 7 -( 3 -( 4 - Methylpiperazine 𠯤 - 1 - base ) propoxy ) Quinazoline - 4 - base ) Phenyl )- 2 -( 3 -( Trifluoromethyl ) Phenyl ) Preparation of acetamide Step 1: 7-(benzyloxy)-4-chloro-6-methoxyquinazoline (1.0 g, 3.33 mmol) and (4-nitrophenyl)boronic acid (0.83 g, 4.99 mmol) were dissolved in 1,4-dimethylamine (12.4 ml) and 2 M sodium carbonate (4.2 ml). Tetra(triphenylphosphine)palladium(0) (1.15 g, 0.99 mmol) was added dropwise, followed by bubbling under nitrogen and stirring overnight at 80°C. After confirming the reaction was complete and adding distilled water, the organic matter was extracted with dichloromethane (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the solution was concentrated under reduced pressure. The concentrated mixture was cured with dichloromethane to obtain the desired compound 7-(benzylmethyloxy)-6-methoxy-4-(4-nitrophenyl)quinazoline (1.25 g, 97%) without further purification, and then subjected to the following reaction. MS (m / z): 388.2 [M+H] + UPLC rt(min): 1.76 Step 2: The 7-(benzylmethyloxy)-6-methoxy-4-(4-nitrophenyl)quinazoline (1.27 g, 3.28 mmol) obtained in Step 1 was dissolved in trifluoroacetic acid (5.0 ml) and stirred at 75 °C for 2 hours. Upon completion of the reaction, the mixture was concentrated under reduced pressure to obtain the desired compound, 6-methoxy-4-(4-nitrophenyl)quinazoline-7-ol 2,2,2-trifluoroacetic acid (0.95 g, 70%), as a solid. The following reactions were carried out without further purification. MS (m / z): 298.1 [M+H] + UPLC rt(min): 1.28 Step 3: Dissolve 2,2,2-trifluoroacetic acid 6-methoxy-4-(4-nitrophenyl)quinazolin-7-ol (2.0 g, 4.86 mmol) and triphenylphosphine (2.55 g, 9.73 mmol) obtained in Step 2 in dichloromethane (48.6 ml), and then add dropwise. N, N-Diisopropylethylamine (1.25 g, 9.73 mmol). After dropwise addition of diisopropyl azodicarbonate (1.97 g, 9.73 mmol) to the reaction mixture, it was stirred overnight at room temperature. Upon completion of the reaction, it was concentrated under reduced pressure and purified by MPLC (EA:HEX = 30–100%) to give the desired compound 7-(3-chloropropoxy)-6-methoxy-4-(4-nitrophenyl)quinazoline (1.82 g, 80% purity, 100% yield). MS (m / z): 374.1 [M+H] + UPLC rt(min): 1.66 Step 4: The 7-(3-chloropropoxy)-6-methoxy-4-(4-nitrophenyl)quinazoline (1.5 g, 4.01 mmol) and 1-methylpiperazine (2.0 g, 20.06 mmol) obtained in Step 3 were dissolved in dimethylacetamide (20.0 ml) and stirred overnight at 80 °C. After confirming the reaction was complete and adding distilled water, the organic matter was extracted with ethyl acetate (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the mixture was concentrated under reduced pressure. The concentrated mixture was dissolved in acetone (10.0 ml), acidified with 4 M HCl / ether, and filtered to obtain the desired compound 6-methoxy-7-(3-(4-methylpiperazine-1-yl)propoxy)-4-(4-nitrophenyl)quinazoline dihydrochloride (1.77 g, 86%). MS(m / z): 438.3 [M+H] + UPLC rt(min): 1.04 Step 5: The 6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)-4-(4-nitrophenyl)quinazoline dihydrochloride (1.77 g, 3.47 mmol) obtained in Step 4 was dissolved in methanol (34 ml), and then Pd / C (0.19 g, 1.734 mmol) was added. The reaction mixture was stirred at 40 °C under hydrogen atmosphere for 1 hour. The reactants were filtered through a diatomaceous earth filter, washed with methanol, and concentrated under reduced pressure to give the desired compound 4-(6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinazoline-4-yl)aniline dihydrochloride (1.6 g, 50%). MS (m / z): 410.3 [M+H] + UPLC rt(min): 0.26 Step 6: Dissolve 2-(3-(trifluoromethyl)phenyl)acetic acid (6.0 mg, 0.31 mmol) and HATU (0.16 g, 0.42 mmol) in dichloromethane (0.7 ml), then add dropwise. N, N-Diisopropylethylamine (0.11 g, 0.83 mmol) was added dropwise, followed by the dropwise addition of 4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)aniline dihydrochloride (0.1 g, 0.21 mmol) obtained in step 5. The mixture was stirred overnight at room temperature. After the reaction was complete, distilled water was added, and the organic matter was extracted with ethyl acetate (×3). The collected organic layer was washed with brine, and the remaining water was removed with sodium sulfate and concentrated under reduced pressure. The concentrated mixture was purified by MPLC (DCM:MeOH=0-10%) to give the desired compound. N-(4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)phenyl)-2-(3-(trifluoromethyl)phenyl)acetamide (3.0 mg, 24%). MS (m / z): 594.4 [M+H] + UPLC rt(min): 1.25 < Example 56> N -( 4 -( 6 - methoxy - 7 -(( 1 - Methylpiperidine - 4 - base ) methoxy ) Quinazoline - 4 - base ) Phenyl )- 2 -( 4 -( Trifluoromethyl ) Phenyl ) Preparation of acetamide Step 1: Dissolve 6-methoxy-4-(4-nitrophenyl)quinazolin-7-ol (5.0 g, 12.16 mmol) of 2,2,2-trifluoroacetic acid obtained in Step 2 of Example 55 and tributyl 4-((toluenesulfonyloxy)methyl)piperidine-1-carboxylic acid (5.84 g, 15.80 mmol) in dimethylformamide (40.0 ml), and then add dropwise. N, N-Diisopropylethylamine (7.86 g, 60.80 mmol) and potassium carbonate (3.36 g, 24.31 mmol). The reaction mixture was stirred overnight at 70 °C, and when the reaction was complete, the solid filtrate was filtered with water to give the desired compound, 4-(((6-methoxy-4-(4-nitrophenyl)quinazolin-7-yl)oxy)methyl)piperidine-1-carboxylic acid tributyl ester (6.20 g, crude, 103%). It was used in the following reaction without further purification. MS (m / z): 495.3 [M+H] + UPLC rt(min): 1.86 Step 2: 6.20 g (12.54 mmol) of tributyl 4-(((6-methoxy-4-(4-nitrophenyl)quinazolin-7-yl)oxy)methyl)piperidin-1-carboxylic acid was dissolved in dichloromethane (62.0 ml), followed by dropwise addition of 4 M HCl (31.3 ml, 125.00 mmol) / dimethyl alkyl. After stirring overnight at room temperature, the solid compound was filtered to give 5.0 g (93%) of the desired compound 6-methoxy-4-(4-nitrophenyl)-7-(piperidin-4-ylmethoxy)quinazolin hydrochloride, which was used in the following reaction without further purification. MS (m / z): 395.2 [M+H] + UPLC rt(min): 1.17 Step 3: Dissolve 6-methoxy-4-(4-nitrophenyl)-7-(piperidin-4-ylmethoxy)quinazoline hydrochloride (0.50 g, 1.16 mmol) and sodium triethoxyborohydride (0.37 g, 1.74 mmol) obtained in Step 2 in 1,4-dimethylethane (5.8 ml), then add formaldehyde (0.94 g, 11.60 mmol) dropwise. N, N-Diisopropylethylamine (0.30 g, 2.32 mmol) was added, and the mixture was stirred overnight at room temperature. After the reaction was complete, distilled water was added, and the organic matter was extracted with dichloromethane (×3). After washing the collected organic layer with brine, the remaining water was removed with sodium sulfate and the mixture was concentrated under reduced pressure to give the desired compound 6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)-4-(4-nitrophenyl)quinazoline. The concentrated mixture (0.45 g, 95%) was used in the following reaction without further purification. MS (m / z): 409.2 [M+H] + UPLCr.t. (min): 1.14 Step 4: 6-Methoxy-7-((1-methylpiperidin-4-yl)methoxy)-4-(4-nitrophenyl)quinazoline (0.45 g, 1.10 mmol) obtained in Step 3 was dissolved in methanol (10.9 ml), and Pd / C (0.05 g, 0.55 mmol) was added. The reaction mixture was stirred for 1 hour at room temperature under hydrogen atmosphere. The reaction mixture was filtered through a diatomaceous earth filter, washed with methanol, and subsequently concentrated under reduced pressure to give the desired compound, 2,2,2-trifluoroacetic acid 4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazoline-4-yl)aniline (0.30 g, 72.3%). MS (m / z): 397.3 [M+H] + UPLCr.t. (min): 0.84 Step 5: Dissolve 2-(4-(trifluoromethyl)phenyl)acetic acid (22.0 mg, 0.11 mmol) and HATU (54.0 mg, 0.14 mmol) in dichloromethane (0.7 ml), then add dropwise. N, N-Diisopropylethylamine (3.7 mg, 0.28 mmol). 2,2,2-Trifluoroacetic acid 4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-yl)aniline (35.0 mg, 0.07 mmol) obtained in step 4 was added to the reaction mixture, and the mixture was stirred overnight at room temperature. After the reaction was complete, distilled water was added, and the organic matter was subsequently extracted with ethyl acetate (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the mixture was concentrated under reduced pressure. After separation and MPLC (DCM:MeOH=0-20%) purification and concentration of the mixture, the desired compound was obtained. N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (20.0 mg, 49.8%). MS (m / z): 565.4 [M+H] + UPLC rt(min): 1.34 Example 55 to Examples 57 to 121 were prepared in a manner similar to Examples 55 and 56, and the compound names, NMR, mass, and UPLC analysis results of Examples 55 to 121 are summarized in Table 2 below. [Table 2] < Example 122> N -( 4 -( 6 -( 2 -( Diethylamino ) ethoxy )- 7 - Methoxyquinazoline - 4 - base ) Phenyl )- 2 -( 4 - Fluorophenyl ) Preparation of acetamide Step 1: 4-chloro-7-methoxyquinazoline-6-yl acetate (0.10 g, 0.40 mmol) and (4-(2-(4-fluorophenyl)acetaminophen)phenyl)boronic acid (0.11 g, 0.40 mmol) were dissolved in 1,4-dimethylamine (1.0 ml) and 1 M sodium carbonate (0.3 ml), followed by dropwise addition of tetra(triphenylphosphine)palladium(0) (0.14 g, 0.12 mmol). After bubbling with nitrogen, the mixture was stirred overnight at 80 °C. After the reaction was complete, the mixture was filtered through a diatomaceous earth filter, washed with methanol, and then concentrated under reduced pressure to give the desired compound, 4-(4-(2-(4-fluorophenyl)acetaminophen)phenyl)-7-methoxyquinazoline-6-yl acetate (250.0 mg, 70% purity, 99% yield). It was used in the following reaction without further purification. MS (m / z): 446.2 [M+H] + UPLC rt(min): 1.55 Step 2: The 4-(4-(2-(4-fluorophenyl)acetaminophen)-7-methoxyquinazoline-6-yl ester (0.25 g, 0.56 mmol) obtained in Step 1 was dissolved in a methanol solution of 7 N (4.0 ml) ammonia, and then stirred at room temperature for 30 minutes. After the reaction was complete, it was filtered through a diatomaceous earth filter, washed with dichloromethane, and concentrated under reduced pressure. The desired compound 2-(4-fluorophenyl)- was obtained as a solid using dichloromethane and diethyl ether. N-(4-(6-hydroxy-7-methoxyquinazoline-4-yl)phenyl)acetamide (0.23 g, 80% purity, 81% yield). It was used in the following reaction without further purification. MS (m / z): 404.1 [M+H] + UPLC rt(min): 1.33 Step 3: The 2-(4-fluorophenyl)- obtained in Step 2 N-(4-(6-hydroxy-7-methoxyquinazoline-4-yl)phenyl)acetamide (0.04 g, 0.10 mmol), 2-chloro-N,N-diethylethane-1-amine hydrochloride (1.9 mg, 0.1 mmol), and potassium carbonate (3.0 mg, 0.22 mmol) were dissolved in acetonitrile (0.3 ml) and distilled water (0.3 ml), and the mixture was stirred at 80 °C for 2 hours. After the reaction was complete, distilled water was added, and the organic matter was extracted with ethyl acetate (×3). The collected organic layer was washed with brine, and the residual water was removed with sodium sulfate and concentrated under reduced pressure. After separation and purification of the concentrated mixture by MPLC (DCM:MeOH=0-10%), the desired compound was obtained. N-(4-(6-(2-(diethylamino)ethoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-fluorophenyl)acetamide (17.0 mg, 34.1%). MS (m / z): 503.3 [M+H] + UPLC rt(min): 1.46 < Example 123> N -( 4 -( 6 -(( 1 - Ethylpiperidine - 4 - base ) Oxygen )- 7 - Methoxyquinazoline - 4 - base ) Phenyl )- 2 -( 4 -( Trifluoromethyl ) Phenyl ) Preparation of acetamide Step 1: 4-((4-chloro-7-methoxyquinazoline-6-yl)oxy)piperidine-1-carboxylic acid tributyl ester (0.30 g, 0.75 mmol) and (4-(2-(4-trifluoromethylphenyl)acetaminophen)phenyl)boronic acid (0.36 g, 1.12 mmol) were dissolved in 1,4-dimethylethane (2.1 ml) and 2 M sodium carbonate (0.9 ml), followed by dropwise addition of tetra(triphenylphosphine)palladium(0) (0.26 g, 0.23 mmol). After bubbling with nitrogen, the mixture was stirred overnight at 80°C. After the reaction was complete, the mixture was filtered through a diatomaceous earth filter and concentrated under reduced pressure to obtain the desired compound, 4-((7-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetaminophen)phenyl)quinazolin-6-yl)oxy)piperidine-1-carboxylic acid tributyl ester (0.26 g, 54.5%). It was used in the following reaction without further purification. MS (m / z): 637.4 [M+H] + UPLC rt(min): 1.87 Step 2: The tributyl 4-((7-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetaminophen)phenyl)quinazolin-6-yl)oxy)piperidin-1-carboxylic acid obtained in Step 1 (0.26 g, 0.41 mmol) was dissolved in dichloromethane (4.1 ml), followed by dropwise addition of trifluoroacetic acid (0.47 g, 4.08 mmol) with stirring overnight at room temperature. After the reaction was complete, the mixture was concentrated under reduced pressure, and then the desired compound, 2,2,2-trifluoroacetic acid, was added. N-(4-(7-methoxy-6-(piperidin-4-yloxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.2 g, 75%) was isolated and purified by preparative HPLC. MS (m / z): 537.3 [M+H] + UPLC rt(min): 1.25 Step 3: 2,2,2-Trifluoroacetic acid obtained in Step 2 N-(4-(7-methoxy-6-(piperidin-4-yloxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (0.03 g, 0.05 mmol) and sodium triacetoxyborohydride (0.02 g, 0.09 mmol) were dissolved in 1,4-dimethylethane (0.5 ml), and then acetaldehyde (3.05 mg, 0.07 mmol) was added dropwise. N, N-Diisopropylethylamine (0.03 g, 0.23 mmol) was reacted and stirred overnight at room temperature. After the reaction was complete, the mixture was concentrated under reduced pressure and purified by preparative HPLC to obtain the desired compound. N-(4-(6-((1-ethylpiperidin-4-yl)oxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide (15.0 mg, 57.6%). MS (m / z): 565.3 [M+H] + UPLC rt(min): 1.29 Example 122 to Examples 124 to 164 were prepared in a manner similar to Examples 122 and 123, and the compound names, NMR, mass, and UPLC analysis results of Examples 122 to 164 are summarized in Table 3 below. [Table 3] < Example 165> 4 -( 6 - methoxy - 7 -( 3 -( 4 - Methylpiperazine 𠯤 - 1 - base ) propoxy ) Quinazoline - 4 - base )- N -( 4 -( Trifluoromethyl ) benzyl ) Preparation of benzylamine Step 1: 7-(benzylmethyloxy)-4-chloro-6-methoxyquinazoline (1 g, 3.33 mmol) and (4-(ethoxycarbonyl)phenyl)boronic acid (0.774 g, 3.99 mmol) were dissolved in 1,4-dimethylethane (11.08 ml) and 1 M sodium carbonate (7.32 ml), followed by dropwise addition of tetra(triphenylphosphine)palladium(0) (0.19 g, 0.17 mmol). After bubbling with nitrogen, the mixture was stirred at 80 °C for 2.5 hours. After the reaction was complete, the mixture was filtered through a diatomaceous earth filter, washed with methanol, concentrated under reduced pressure, and then separated and purified by MPLC (EA:HEX=0-80%) to give the desired compound ethyl 4-(7-(benzylmethyloxy)-6-methoxyquinazoline-4-yl)benzoate (850.0 mg, yield 61.7%). MS(m / z): 414.9 [M+H] + UPLC rt(min): 2.07 Step 2: The ethyl 4-(7-(benzylmethyloxy)-6-methoxyquinazoline-4-yl)benzoate (1.34 g, 3.23 mmol) obtained in Step 1 was dissolved in trifluoroacetic acid (4.74 ml) and stirred overnight at 80 °C. Upon completion of the reaction, the mixture was concentrated under reduced pressure to obtain the desired compound, ethyl 4-(7-hydroxy-6-methoxyquinazoline-4-yl)benzoate (0.9 g, 90%), in solid form. The following reactions were carried out without further purification. MS (m / z): 325.0 [M+H] + UPLC rt(min): 1.57 Step 3: Dissolve ethyl 4-(7-hydroxy-6-methoxyquinazoline-4-yl)benzoate (0.56 g, 1.33 mmol) and potassium carbonate (0.733 g, 5.30 mmol) obtained in Step 2 in acetonitrile (3.79 ml), and then add dropwise. N, N-Diisopropylethylamine (0.857 g, 6.63 mmol). After dropwise addition of 1-(3-chloropropyl)-4-methylpiperazolin-4-yl hydrochloride (0.993 g, 3.98 mmol) to the reaction mixture, the mixture was stirred overnight at 70 °C. Upon completion of the reaction, the mixture was concentrated under reduced pressure and purified by MPLC (DCM:MeOH=0-20%) to give the desired compound ethyl 4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)benzoate (0.29 g, yield 47.1%). MS (m / z): 465.3 [M+H] + UPLC rt(min): 1.32 Step 4: Ethyl 4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazoline-4-yl)benzoate (0.29 g, 0.624 mmol) obtained in Step 3 and lithium hydroxide hydrate (52.4 mg, 1.248 mmol) were dissolved in methanol (1.24 ml) and distilled water (1.24 ml), and stirred overnight at room temperature. After the reaction was complete, 1 N hydrochloric acid and distilled water were added, and the organic matter was extracted with ethyl acetate (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the mixture was concentrated under reduced pressure. After concentration, the desired compound 4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazoline-4-yl)benzoic acid (180 mg, 66%) was obtained. MS (m / z): 437.2 [M+H] + UPLC rt(min): 1.09 Step 5: Dissolve (4-(trifluoromethyl)phenyl)methylamine (108 mg, 0.61 mmol) and HATU (235.0 mg, 0.61 mmol) in dichloromethane (0.8 ml), then add dropwise. N, N-Diisopropylethylamine (133 mg, 1.03 mmol). 4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazolin-4-yl)benzoic acid (108 mg, 0.619 mmol), obtained in step 4, was added to the reaction mixture, and the mixture was stirred at room temperature for 2 hours. After the reaction was complete, distilled water was added, and the organic matter was subsequently extracted with ethyl acetate (×3). The collected organic layer was washed with brine, the remaining water was removed with sodium sulfate, and the mixture was concentrated under reduced pressure. After separation and purification of the concentrated mixture by MPLC (DCM:MeOH=0-20%), the desired compound 4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazolin-4-yl)- N-(4-(trifluoromethyl)benzyl)benzamide (21 mg, 17.1%). MS (m / z): 594.3 [M+H] + UPLC rt(min): 1.52 Example 165 to Examples 166 to 167 were prepared in a manner similar to that of Example 165, and the compound names, NMR, mass, and UPLC analysis results of Examples 165 to 167 are summarized in Table 4 below. [Table 4] < Example 168> 1 -( 4 - chlorine - 3 -( Trifluoromethyl ) Phenyl )- 3 -( 4 -( 6 - methoxy - 7 -( 3 -( 4 - Methylpiperazine 𠯤 - 1 - base ) propoxy ) Quinazoline - 4 - base ) Phenyl ) Preparation of urea Step 1: Dissolve 4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)aniline (128 mg, 0.314 mmol) and 1,1'-carbonyldiimidazole (CDI) (102 mg, 0.628 mmol) in dichloromethane (0.8 ml), then add dropwise. N, N-Diisopropylethylamine (60.9 mg, 0.471 mmol). After stirring at room temperature for 1 hour and the reaction was complete, distilled water was added and the organic matter was extracted with dichloromethane (×3). The collected organic layer was washed with brine, the residual water was removed with sodium sulfate, and the solution was concentrated under reduced pressure to obtain the desired compound. N-(4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazolin-4-yl)phenyl)-1 H-Imidazol-1-methamide (136 mg, 86%). It was used in the following reaction without prior purification. MS (m / z): 466.0 [M+H] + UPLC rt(min): 1.12 Step 2: Obtain the item from Step 1 N-(4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazolin-4-yl)phenyl)-1 H-Imidazol-1-methamide (136 mg, 0.271 mmol) was dissolved in dichloromethane (0.8 ml) and then added dropwise. N, N-Diisopropylethylamine (60.9 mg, 0.471 mmol) and 4-chloro-3-(trifluoromethyl)aniline (80 mg, 0.407 mmol). The reaction was stirred at 50 °C for 1 hour. After the reaction was complete, distilled water was added and the organic matter was extracted with dichloromethane (×3). The collected organic layer was washed with brine, and the remaining water was removed with sodium sulfate. The mixture was concentrated under reduced pressure, and the desired compound 1-(4-chloro-3-(trifluoromethyl)phenyl)-3-(4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)phenyl)urea (38.7 mg, 22.6%) was separated and purified by preparative HPLC. MS (m / z): 629.2 [M+H] + UPLC rt(min): 1.60 Example 168 to Example 169 was prepared in a similar manner to Example 168, and the compound names, NMR, mass, and UPLC analysis results of Examples 168 to 169 are summarized in Table 5 below. [Table 5] Experimental Examples 1 : Evaluation targeting PDGFR - α , PDGFR - β , c - KIT To evaluate the inhibitory activity of the compounds synthesized according to the above examples against PDGFR-α (wt), PDGFR-β (wt), c-KIT (wt), and c-KIT (D816V) kinases, the following methods were performed. The compounds of the examples were reacted with purified human PDGFR-α (wt) (Signalchem ​​#P12-18G), human PDGFR-β (wt) (Signalchem ​​#P13-11G), human c-KIT (wt) (Signalchem ​​#K06-11BG), and human c-KIT (D816V) (Signalchem ​​#C06-12LG) enzymes, and the enzyme inhibitory activity was evaluated by the following methods. The reaction buffer was prepared as 40 mM Tris-HCl pH 7.4 and 20 mM MgCl₂. 2. A combination of 0.5 mg / ml BSA and 50 μM DTT was used, and all tests were performed on reaction buffer. The compounds were serially diluted from 10 mM DMSO stock solution in 12 steps, and enzyme activity was measured at final compound concentrations from 10 to 0.00005645 μM. During the assay, human PDGFR-α (wt), human PDGFR-β (wt), human c-KIT (wt), and human c-KIT (D816V) enzymes were reacted with purified ATP and enzyme acceptors at appropriate concentrations at 25°C for 1 to 2 hours, followed by in vitro ADP-Glo TM Enzyme activity was confirmed by kinase assay (Promega). The enzyme activity reaction solution, ADP-Glo ​​reaction solution, and enzyme activity detection solution were reacted in a 2:2:1 ratio, and the inhibition of enzyme activity was measured by luminosclenescence. Based on the enzyme activity fluorescence of the untreated solvent control group, the degree of enzyme activity inhibition was calculated according to the treatment concentration of each compound, and the concentration of each compound that inhibited 50% of enzyme activity was determined as the IC50. 50 The (nM) value was obtained using GraphPad Prism 8.3.0 (GraphPad software Inc., San Diego). The results are shown in Table 6 below. (A: IC) 50 ≤ 50nM; B: 50nM < IC 50 ≤ 100nM; C: 100nM < IC 50 ≤ 500nM; D: IC 50 > 500 nM). [Table 6] As shown in Table 6, the compounds of the present invention are confirmed to have the ability to inhibit the activity of PDGFR-α, PDGFR-β, c-KIT(wt), and c-KIT(D816V) kinases. This indicates that the compounds of the present invention can be effectively used for the prevention or treatment of diseases associated with PDGFR-α, PDGFR-β, c-KIT(wt), or c-KIT(D816V). Experimental Examples 2 : Evaluation of Ba / F3 Cell proliferation inhibition activity was achieved by using Ba / F3-TEL-PDGFRα(WT), Ba / F3-TEL-PDGFRβ(WT), Ba / F3-c-KIT(D816V) (Kyinno, #KC-0138), c-KIT V560G / D816V, and c-KIT D814Y at a concentration of 3 × 10⁻⁶. 3 100 μl / well was seeded into a white 96-well dish with a transparent bottom. Culture solutions containing 12 sequentially diluted (3-fold) concentrations (0.00001–2 mM) of compounds and DMSO control were added at 0.5 μl / well each to a final concentration of 0.00005–10 μM, and then incubated in CO2. 2. Incubate at 37°C for 72 hours in an incubator. After 72 hours, remove the compound-treated trays and treat with 100 μl / well CellTiter-Glo® (Promega) solution, followed by thorough mixing. After thorough mixing for approximately 10 minutes at room temperature, measure fluorescence using a microplate reader. Data are presented as a percentage based on the ratio of the medium to the treated cells. GI was calculated using GraphPad Prism 8.3.0 (GraphPad software Inc., San Diego). 50 (nM) value. The inhibitory activity of PDGFR-α, PDGFR-β, c-KIT (D816V), c-KIT V560G / D816V and c-KIT D814Y on Ba / F3 was measured as described above and is shown in Table 7 below (A: GI). 50 ≤ 200nM; B: 200nM < GI 50 ≤ 500nM; C:GI 50 > 500 nM). [Table 7] As shown in Table 7, the compounds of the present invention exhibit activity in inhibiting the proliferation of overactivated cell lines of PDGFR-α, PDGFR-β, c-KIT(D816V), c-KIT V560G / D816V and c-KIT D814Y. Experimental Examples 3 : Evaluation of Inhibitory Activity Against Various Kinases: The activities of the compounds according to the present invention against various enzymes were evaluated. Specifically, the enzyme selectivity of the compounds in Examples 3, 9, and 83 above was measured by DiscoverX, and experiments were conducted using the scanMAX™ kinase analysis panel. In this paper, a solution prepared by dissolving the compound in DMSO at a concentration of 1 μM was used as the drug for enzyme treatment, and the control percentage (control %) was determined by the method of Equation 1 below, and the results are shown in Table 8 below. [Equation 1] In this equation, the positive control group and the negative control group refer to the compound exhibiting 0% of the control percentage and DMSO exhibiting 100% of the control percentage, respectively. In this document, when the calculated percentage value of each enzyme is less than 35%, inhibitory activity against the enzyme is determined. Therefore, among the series of enzymes tested, the enzymes exhibiting inhibitory activity of the compounds of the present invention and their control percentages are summarized and shown in Table 8 below. (◎: less than 10%; ○: 10% or more up to less than 35%). [Table 8] Since the specific details of the invention have been described above, those skilled in the art will understand that the specific techniques are merely preferred embodiments, and the scope of the invention is not limited thereto. Therefore, the essential scope of the invention will be defined by the appended claims and their equivalents.

Claims

1. A compound represented by the following chemical formula 1, its stereoisomer or a pharmaceutically acceptable salt thereof, [chemical formula 1] in which R1 is -(CH2)m-RX or -(C=O)-RX, and R2 is -(C1-C6)alkyl; RX is -NRARB, heterocyclic alkyl, or heteroaryl {wherein at least one H in the heterocyclic alkyl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)alkyl-O-(C1-C6)alkyl, -(C=O)-(C1-C6)alkyl, -(C=O)-O-(C1-C6)alkyl, -NRCRD, -(=O)-, cycloalkyl, or benzyl, [wherein at least one H in the benzyl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)alkoxy, -(C1-C6)haloalkyl, or halo]; at least one H in the heteroaryl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)haloalkyl, or halo}; RA and RB are each independently -H, -(C1-C6)alkyl, cycloalkyl, heterocycloalkyl, aryl, or heteroaryl {wherein, At least one H in the cycloalkyl, heterocycloalkyl, aryl, or heteroaryl ring may be substituted with a -(C1-C6)alkyl group; RC and RD are each independently -H or -(C1-C6)alkyl; m is 0, 1, 2, 3, or 4; R3 is -H, -(C1-C6)alkyl, or -halo; L is -NH(C=O)-L1-(CH2)n-L2- or -(C=O)NH-L1-(CH2)n-L2-; L1 and L2 are each independently -CRERF-, -C(=O)NH-, or empty; RE and RF are each independently -H, -(C1-C6)alkyl, or -NH2, or RE and RF may combine with carbon to form a -(C3-C6)cycloalkyl group; n is 0, 1, 2, or 3; Z is an aryl, heteroaryl, heterohydroaryl, heterocyclic alkyl, or -(C2-C6)alkenyl ring {wherein, at least one H in the aryl, heteroaryl, or heterohydroaryl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)haloalkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)cyanoalkyl, -CN, -(C1-C6)alkoxy, or -halo; at least one H in the heterocyclic alkyl ring may be substituted with -(C1-C6)alkyl}.

2. The compound represented by Formula 1, its stereoisomers, or a pharmaceutically acceptable salt thereof, as claimed in claim 1, wherein R1 is -(CH2)m-RX or -(C=O)-RX, and R2 is -(C1-C6)alkyl; RX is -NRARB, heterocyclic alkyl, or heteroaryl {wherein, at least one H in the heterocyclic alkyl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)alkyl-O-(C1-C6)alkyl, -(C=O)-(C1-C6)alkyl, -(C=O)-O-(C1-C6)alkyl, -NRCRD, -(=O)-, cycloalkyl, or benzyl [wherein, At least one H in the benzyl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)alkoxy, -(C1-C6)haloalkyl or haloyl; and at least one H in the heteroaryl ring may be substituted with -(C1-C6)haloalkyl; RA and RB are each independently -H, -(C1-C6)alkyl, cycloalkyl or heteroaryl {wherein at least one H in the cycloalkyl or heteroaryl ring may be substituted with -(C1-C6)alkyl}; RC and RD are each independently -H or -(C1-C6)alkyl; m is 0, 1, 2, 3 or 4; R3 is -H, -(C1-C6)alkyl or -haloyl; L is -NH(C=O)-L1-(CH2)n-L2- or -(C=O)NH-L1-(CH2)n-L2-; L1 and L2 are each independently -CRERF- or empty; RE and RF are each independently -H, -(C1-C6)alkyl or -NH2, or RE and RF combine with carbon to form -(C3-C6)cycloalkyl; n is 0, 1, 2 or 3; Z is phenyl, 5-10-membered heteroaryl, 5-10-membered heterohydroaryl, 5-10-membered heterocycloalkyl or -(C2-C6)alkenyl {wherein, at least one H in the phenyl, 5-10-membered heteroaryl or 5-10-membered heterohydroaryl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)haloalkyl, -CN, -(C1-C6)alkoxy or -halo; at least one H in the 5-10-membered heterocycloalkyl ring may be substituted with -(C1-C6)alkyl}.

3. The compound represented by Formula 1, its stereoisomers, or its pharmaceutically acceptable salts as claimed in claim 1, wherein R1 is -(CH2)m-RX or -(C=O)-RX, and R2 is -(C1-C6)alkyl; RX is -NRARB, heterocyclic alkyl, or heteroaryl {wherein, the heterocyclic alkyl is monocyclic, spirocyclic, bridged, or fused-ring, and at least one H in the heterocyclic alkyl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)hydroxyalkyl, -(C1-C6)alkyl-O-(C1-C6)alkyl, -(C=O)-(C1-C6)alkyl, -(C=O)-O-(C1-C6)alkyl, -NRCRD, -(=O)-, cycloalkyl, or benzyl [wherein, At least one H in the benzyl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)alkoxy, -(C1-C6)haloalkyl or haloalkyl; and at least one H in the heteroaryl ring may be substituted with -(C1-C6)haloalkyl; RA and RB are each independently -H, -(C1-C6)alkyl, cycloalkyl or heteroaryl {wherein at least one H in the cycloalkyl or heteroaryl ring may be substituted with -(C1-C6)alkyl}; RC and RD are each independently -H or -(C1-C6)alkyl; m is 0, 1, 2 or 3.

4. The compound represented by Formula 1, its stereoisomers or its pharmaceutically acceptable salts as claimed in claim 1, wherein the compound represented by Formula 1 is represented by the following Formula 2: [Formula 2] In Formula 2, R3 is -H, -(C1-C6)alkyl or -halogen.

5. The compound represented by Formula 1, its stereoisomers or its pharmaceutically acceptable salts as claimed in claim 1, wherein L is -NH(C=O)-L1-(CH2)n-L2- or -(C=O)NH-L1-(CH2)n-L2-; L1 and L2 are each independently -CRERF- or empty; RE and RF are each independently -H, -(C1-C6)alkyl or -NH2, or RE and RF combine with carbon to form -(C3-C6)cycloalkyl; n is 0, 1, 2 or 3.

6. A compound represented by Formula 1, its stereoisomers, or a pharmaceutically acceptable salt thereof, as claimed in claim 1, wherein Z is phenyl, 5-10-membered heteroaryl, 5-10-membered heterohydroaryl, 5-10-membered heterocycloalkyl, or -(C2-C6)alkenyl {wherein, At least one H in the phenyl, the 5-10 member heteroaryl, or the 5-10 member heterohydroaryl ring may be substituted with -(C1-C6)alkyl, -(C1-C6)haloalkyl, -CN, -(C1-C6)alkoxy, or -halo; at least one H in the 5-10 member heterocyclic alkyl ring may be substituted with -(C1-C6)alkyl.

7. A compound, its stereoisomer, or a pharmaceutically acceptable salt thereof, wherein the compound is selected from the group consisting of: (1) N-(4-(7-(2-(diethylamino)ethoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (2) N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)oxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (3) N-(4-(6-methoxy-7-(2-(4-methylpiperidin-1-yl)ethoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (4) (5) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (6) N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (7) 2-amino-N-(4-(7-(7-(benzylmethyloxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-fluorophenyl)propionic acid; (8) 2-Amino-2-(4-fluorophenyl)-N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)propionic acid; (9) N-(4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (10) 2-Amino-2-(4-fluorophenyl)-N-(4-(7-isobutoxy-6-methoxyquinazoline-4-yl)phenyl)propionic acid; (11) N-(4-(7-(3-(diethylamino)propoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (12) N-(4-(7-(benzylmethyloxy)-6-methoxyquinazoline-4-yl)phenyl)-2-methyl-2-(4-(trifluoromethyl)phenyl)propionic acid; (13) N-(4-(7-hydroxy-6-methoxyquinazoline-4-yl)phenyl)-2-methyl-2-(4-(trifluoromethyl)phenyl)propionic acid; (14) 3-(((6-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamino)phenyl)quinazoline-7-yl)oxy)methyl)piperidine-1-carboxylic acid tributyl ester; (15) 4-(((6-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamino)phenyl)quinazoline-7-yl)oxy)methyl)piperidine-1-carboxylic acid tributyl ester;(16) N-(4-(6-methoxy-7-(piperidin-3-ylmethoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (17) N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (18) N-(4-(7-((1-ethylpiperidin-3-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (19) 6-(3-((6-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetaminophen)phenyl)quinazolin-7-yl)oxy)propoxy)-2,6-diazaspiro[3.3]heptane-2-carboxylic acid tributyl ester; (20) N-(4-(7-(3-(2,6-diazaspiro[3.3]heptane-2-yl)propoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (21) N-(4-(7-(3-(6-ethyl-2,6-diazaspiro[3.3]heptane-2-yl)propoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (22) N-(4-(7-(3-(3-(dimethylamino)azacyclobutane-1-yl)propoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (23) N-(4-(7-(3-chloropropoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (24) N-(4-(7-(azacyclobutane-3-yloxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (25) N-(4-(7-(3-(cyclopropylamino)propoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (26) N-(4-(6-methoxy-7-(3-(((1-methyl-1H-pyrazol-4-yl)amino)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (27) N-(4-(6-methoxy-7-((1-(4-methoxybenzyl)azacyclobut-3-yl)oxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (28) N-(4-(6-methoxy-7-((1-(2-methoxyethyl)azacyclobut-3-yl)oxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (29) N-(4-(6-methoxy-7-(pyridin-3-ylmethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide;(30) N-(4-(7-(2-(1H-pyrazol-1-yl)ethoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (31) N-(4-(6-methoxy-7-(3-((1R,4R)-5-methyl-2,5-diazabicyclo[2.2.1]heptane-2-yl)propoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (32) N-(4-(6-methoxy-7-(3-((1S,4S)-5-methyl-2,5-diazabicyclo[2.2.1]heptane-2-yl)propoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (33) N-(4-(7-(3-(hexahydropyrrolo[1,2-a]pyrrolidone-2(1H)-yl)propoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (34) N-(4-(6-methoxy-7-(3-(3-(trifluoromethyl)-5,6-dihydro-[1,2,4]triazol[4,3-a]pyrrolidone-7(8H)-yl)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (35) (R)-3-(((6-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamide)phenyl)quinazolin-7-yl)oxy)methyl)pyrrolidone-1-carboxylic acid tributyl ester; (36) (S)-3-(((6-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetaminophen)phenyl)quinazolin-7-yl)oxy)methyl)pyrrolidin-1-carboxylic acid tributyl ester; (37) N-(4-(6-methoxy-7-(3-(3-methyl-3,6-diazabicyclo[3.1.1]heptane-6-yl)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (38) (R)-N-(4-(6-methoxy-7-(pyrrolidin-3-ylmethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (39) (S)-N-(4-(6-methoxy-7-(pyrrolidin-3-ylmethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (40) (R)-N-(4-(7-((1-ethylpyrrolidin-3-yl)methoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (41) (S)-N-(4-(7-((1-ethylpyrrolidin-3-yl)methoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide;(42) N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-3-yl)methoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (43) N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (44) N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (48) 2-(furan-2-yl)-N-(4-(6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinazoline-4-yl)phenyl)acetamide; (49) N-(4-(6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinazoline-4-yl)-2-methylphenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (50) N-(2-fluoro-4-(6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (51) N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazolin-4-yl)phenyl)-2-(thiazolin-4-yl)acetamide; (52) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(2-fluoro-4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazolin-4-yl)phenyl)acetamide; (53) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazolin-4-yl)-2-methylphenyl)acetamide; (54) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazoline-4-yl)phenyl)acetamide; (55) N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazoline-4-yl)phenyl)-2-(3-(trifluoromethyl)phenyl)acetamide; (56) N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (57) N-(4-(6,7-bis(2-methoxyethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide;(58) 2-amino-N-(4-(6,7-bis(2-methoxyethoxy)quinazoline-4-yl)phenyl)-2-(4-fluorophenyl)propionic acid; (59) N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (60) N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)-2-(3-(trifluoromethyl)phenyl)acetamide; (61) 2-(4-isopropyl-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)acetamide; (62) 2-(4-(tributyl)-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazolin-4-yl)phenyl)acetamide; (63) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (64) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(3-(trifluoromethyl)phenyl)acetamide; (65) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-isopropyl-1H-1,2,3-triazol-1-yl)acetamide; (66) 2-(4-(tributyl)-1H-1,2,3-triazol-1-yl)-N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)acetamide; (67) 2-(4-isopropyl-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazoline-4-yl)phenyl)acetamide; (68) 2-(4-(tributyl)-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazoline-4-yl)phenyl)acetamide; (69) 2-(6-chloropyridin-3-yl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)acetamide; (70) 2-(6-chloropyridin-3-yl)-N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)acetamide; (71) N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazolin-4-yl)phenyl)-3-phenylpropionamine;(72) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-3-phenylpropionic acid; (73) (R)-N-(4-(6-methoxy-7-(piperidin-3-ylmethoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (74) (R)-N-(4-(7-((1-ethylpiperidin-3-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (75) (S)-N-(4-(6-methoxy-7-(piperidin-3-ylmethoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (76) (S)-N-(4-(7-((1-ethylpiperidin-3-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (77) 2-(4-chloro-3-(trifluoromethyl)phenyl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)acetamide; (78) 2-(4-chloro-3-(trifluoromethyl)phenyl)-N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)acetamide; (79) 2-(3-fluoro-4-(trifluoromethyl)phenyl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)acetamide; (80) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(3-fluoro-4-(trifluoromethyl)phenyl)acetamide; (81) N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazoline-4-yl)phenyl)-2-(6-methoxypyridin-3-yl)acetamide; (82) 2-(4-chloro-3-(trifluoromethyl)phenyl)-N-(4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazoline-4-yl)phenyl)acetamide; (83) 2-(4-cyanophenyl)-N-(4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazoline-4-yl)phenyl)acetamide; (84) N-(4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazoline-4-yl)phenyl)-2-(thiophen-3-yl)acetamide; (85) 2-(2,3-Dihydrobenzofuran-5-yl)-N-(4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)phenyl)acetamide;(86) N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazolin-4-yl)phenyl)-2-(piperidin-4-yl)acetamide; (87) N-(4-(6-methoxy-7-(3-(4-methylpiperidin-1-yl)propoxy)quinazolin-4-yl)phenyl)but-3-enylamine; (88) 2-(4-fluorophenyl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazolin-4-yl)phenyl)-2-methylpropionic acid; (89) 2-(4-fluorophenyl)-N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazolin-4-yl)phenyl)-2-methylpropionic acid; (90) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-fluorophenyl)-2-methylpropane; (91) 1-(4-fluorophenyl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazoline-4-yl)phenyl)cyclopropane-1-methylamine; (92) 1-(4-fluorophenyl)-N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)cyclopropane-1-methylamine; (93) N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-1-(4-fluorophenyl)cyclopropane-1-methamide; (94) 2-(4-isopropyl-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)acetamide; (95) 2-(4-(tributyl)-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)acetamide; (96) N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazolin-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (97) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(4-(6-methoxy-7-(piperidin-4-ylmethoxy)quinazolin-4-yl)phenyl)acetamide; (98) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazolin-4-yl)phenyl)acetamide;(99) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(4-(7-((1-ethylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)acetamide; (100) N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)-2-(6-methoxypyridin-3-yl)acetamide; (101) N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (102) N-(4-(7-((1-acetylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (103) N-(4-(7-((1-acetylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(6-methoxypyridin-3-yl)acetamide; (104) N-(4-(7-((1-acetylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (105) 2-(4-Isopropyl-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-yl)phenyl)acetamide; (106) 2-(4-(tributyl)-1H-1,2,3-triazol-1-yl)-N-(4-(6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-yl)phenyl)acetamide; (107) N-(4-(7-((1-acetylpiperidin-4-yl)methoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-isopropyl-1H-1,2,3-triazol-1-yl)acetamide; (108) N-(4-(7-((1-acetylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(tributyl)-1H-1,2,3-triazol-1-yl)acetamide; (109) N-(4-(7-((1-ethylpiperidin-3-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(6-methoxypyridin-3-yl)acetamide; (110) N-(4-(7-((1-ethylpiperidin-3-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (111) N-(4-(7-(((1-ethylpiperidin-3-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-isopropyl-1H-1,2,3-triazol-1-yl)acetamide;(112) 2-(4-(tributyl)-1H-1,2,3-triazol-1-yl)-N-(4-(7-((1-ethylpiperidin-3-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)acetamide; (113) 2-(6-chloropyridin-3-yl)-N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)acetamide; (114) N-(4-(6-methoxy-7-((1-(2-methoxyethyl)piperidin-4-yl)methoxy)quinazoline-4-yl)phenyl)-4-phenylbutyramide; (115) N-(4-(7-((1-isopropylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (116) N-(4-(7-((1-isopropylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(6-methoxypyridin-3-yl)acetamide; (117) N-(4-(6-methoxy-7-(2-methoxyethoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (118) N-(4-(6-methoxy-7-(2-methoxyethoxy)quinazoline-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (119) 2-(4-(tripropylbutyl)-1H-1,2,3-triazol-1-yl)-N-(4-(7-((1-isopropylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)acetamide; (120) 2-(4-isopropyl-1H-1,2,3-triazol-1-yl)-N-(4-(7-((1-isopropylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)acetamide; (121) N-(4-(7-((1-isopropylpiperidin-4-yl)methoxy)-6-methoxyquinazoline-4-yl)phenyl)-2-(6-(trifluoromethyl)pyridin-3-yl)acetamide; (122) N-(4-(6-(2-(diethylamino)ethoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-fluorophenyl)acetamide; (123) N-(4-(6-((1-ethylpiperidin-4-yl)oxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (124) 2-(4-fluorophenyl)-N-(4-(6-hydroxy-7-methoxyquinazoline-4-yl)phenyl)acetamide; (125) (R)-N-(4-(7-methoxy-6-((tetrahydrofuran-3-yl)oxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide;(126) N-(4-(7-methoxy-6-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (127) N-(4-(6-(3-(4-cyclopropylpiperazolin-1-yl)propoxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (128) N-(4-(6-(3-(4-acetylpiperazolin-1-yl)propoxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (129) N-(4-(7-methoxy-6-(3-morpholinylpropoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (130) 3-(((7-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamide)phenyl)quinazolin-6-yl)oxy)methyl)piperidine-1-carboxylic acid tributyl ester; (131) N-(4-(7-methoxy-6-(2-(4-methylpiperidine-1-yl)ethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (132) 4-Methylpiperidin-1-carboxylic acid 7-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamino)phenyl)quinazoline-6-yl ester; (133) N-(4-(7-methoxy-6-(piperidin-3-ylmethoxy)quinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (134) N-(4-(6-((1-ethylpiperidin-3-yl)methoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (135) 3-((7-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamino)phenyl)quinazoline-6-yl)oxy)azacyclobutane-1-carboxylic acid tributyl ester; (136) 3-((7-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamino)phenyl)quinazoline-6-yl)oxy)pyrrolidine-1-carboxylic acid tributyl ester; (137) 4-((7-methoxy-4-(4-(2-(4-(trifluoromethyl)phenyl)acetamino)phenyl)quinazoline-6-yl)oxy)piperidine-1-carboxylic acid tributyl ester; (138) N-(4-(6-(azacyclobut-3-yloxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetaminophen; (139) N-(4-(7-methoxy-6-(pyrrolidin-3-yloxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide;(140) N-(4-(7-methoxy-6-(piperidin-4-yloxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (141) N-(4-(7-(3-(4-acetylpiperidin-1-yl)propoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (142) N-(4-(7-(3-(4-cyclopropylpiperidin-1-yl)propoxy)-6-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (143) N-(4-(6-methoxy-7-(3-(4-methyl-3-yl-piperazolin-1-yl)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (144) N-(4-(6-((1-ethylaziridine-3-yl)oxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (145) N-(4-(6-((1-ethylpyrrolidin-3-yl)oxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (146) N-(4-(7-methoxy-6-(piperidin-4-ylmethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (147) N-(4-(6-((1-ethylpiperidin-4-yl)methoxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (148) N-(4-(6-(3-(2,6-diazaspiro[3.3]heptane-2-yl)propoxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (149) N-(4-(6-(3-(6-ethyl-2,6-diazaspiro[3.3]heptane-2-yl)propoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (150) N-(4-(6-(3-(3,3-bis(hydroxymethyl)azacyclobut-1-yl)propoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (151) N-(4-(6-(3-(7-oxo-2-azaspiro[3.5]nonane-2-yl)propoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (152) N-(4-(6-(3-(3-(dimethylamino)azacyclobut-1-yl)propoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide;(153) N-(4-(7-methoxy-6-(oxacyclobut-3-yloxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (154) N-(4-(6-(3-(cyclopropylamino)propoxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (155) N-(4-(7-methoxy-6-(3-((1-methyl-1H-pyrazol-4-yl)amino)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (156) (S)-N-(4-(7-methoxy-6-((tetrahydrofuran-2-yl)oxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (157) N-(4-(7-methoxy-6-(pyridin-3-ylmethoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (158) N-(4-(7-methoxy-6-(3-((1S,4S)-5-methyl-2,5-diazabicyclo[2.2.1]heptane-2-yl)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (159) N-(4-(7-methoxy-6-(3-((1R,4R)-5-methyl-2,5-diazabicyclo[2.2.1]heptane-2-yl)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (160) N-(4-(7-methoxy-6-(3-(pyrrolidin-1-yl)propoxy)quinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (161) N-(4-(6-(3-(hexahydropyrrolo[1,2-a]pyrrolidone-2(1H)-yl)propoxy)-7-methoxyquinazolin-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (162) N-(4-(6-(3-(2-oxa-6-azaspiro[3.3]heptane-6-yl)propoxy)-7-methoxyquinazoline-4-yl)phenyl)-2-(4-(trifluoromethyl)phenyl)acetamide; (163) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(2-fluoro-4-(6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinazoline-4-yl)phenyl)acetamide; (164) 2-(benzo[d][1,3]m-dioxacyclopenten-5-yl)-N-(4-(6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinazoline-4-yl)-2-methylphenyl)acetamide; (165) 4-(6-methoxy-7-(3-(4-methylpiperazolin-1-yl)propoxy)quinazolin-4-yl)-N-(4-(trifluoromethyl)benzyl)benzamide;(166) N-(benzo[d][1,3]m-dioxacyclopenten-5-ylmethyl)-4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazolin-4-yl)benzamide; and (167) N-(3,4-difluorobenzyl)-4-(6-methoxy-7-(3-(4-methylpiperyl-1-yl)propoxy)quinazolin-4-yl)benzamide.

8. A pharmaceutical composition comprising a compound, a stereoisomer thereof, or a pharmaceutically acceptable salt thereof, as claimed in any one of claims 1 to 7.

9. A pharmaceutical composition for the prevention or treatment of one or more diseases selected from the group consisting of: cancer, mast cell-related diseases, fibrotic diseases, neurological diseases, atherosclerosis, and pulmonary hypertension, wherein the pharmaceutical composition comprises a compound, a stereoisomer thereof, or a pharmaceutically acceptable salt thereof as an active ingredient, as claimed in any one of claims 1 to 7.

10. The pharmaceutical composition of claim 9, wherein the cancer is selected from one or more of the following groups: lung cancer, peritoneal cancer, skin cancer, endocrine gland cancer, soft tissue sarcoma, urethral cancer, leukemia, gastrointestinal cancer, pancreatic cancer, cervical cancer, ovarian cancer, bladder cancer, liver tumor, breast cancer, uterine cancer, kidney cancer, prostate cancer, vulvar cancer, head and neck cancer, brain cancer, osteosarcoma, neuroblastoma, and germ cell tumor.

11. The pharmaceutical composition of claim 9, wherein the fibrotic disease is selected from any one or more of the following groups: systemic sclerosis, pulmonary fibrosis, liver fibrosis, cirrhosis, renal fibrosis, myelofibrosis, myocardial fibrosis, sarcoidosis, keloid, burn-induced hypertrophic scar, proliferative retinopathy, glaucoma, cataract, posterior capsular opacification, angioplasty, restenosis following vascular surgery or vascular injury, cystic fibrosis, and Marfan syndrome.

12. A pharmaceutical composition for the prevention or treatment of c-KIT or PDGFR-related diseases, comprising, as an active ingredient, a compound, a stereoisomer thereof, or a pharmaceutically acceptable salt thereof, as claimed in any one of claims 1 to 7.

13. The pharmaceutical composition of claim 12, wherein the composition inhibits any or more of the following components: PDGFR-α, PDGFR-β, c-KIT (D816V), c-KIT V560G / D816V and c-KIT D814Y.

14. The pharmaceutical composition of claim 9, wherein the cancer is selected from one or more of the following groups: squamous cell carcinoma, small cell lung cancer, non-small cell lung cancer, lung adenocarcinoma, melanoma of the skin or eye, rectal cancer, perianal adenocarcinoma, esophageal cancer, small bowel cancer, thyroid cancer, parathyroid cancer, adrenal cancer, chronic or acute leukemia, lymphocytic lymphoma, gastric cancer, glioblastoma, liver cancer, colon cancer, colorectal cancer, endometrial cancer, salivary gland cancer, and gastrointestinal stromal tumor.

15. The pharmaceutical composition of claim 9, wherein the cancer is selected from one or more of the following: hepatocellular carcinoma and squamous cell carcinoma of the lung.

16. Use of a compound, its stereoisomer, or a pharmaceutically acceptable salt thereof as claimed in any one of claims 1 to 7, for the preparation of an agent for the treatment or prevention of one or more diseases selected from the group consisting of: cancer, mast cell-related diseases, fibrotic diseases, neurological diseases, atherosclerosis, and pulmonary hypertension.

17. Use of a compound, its stereoisomer, or a pharmaceutically acceptable salt thereof as claimed in any one of claims 1 to 7, for the preparation of a medicament for the treatment or prevention of c-KIT or PDGFR-related diseases.