Application of ensatinib or pharmaceutically acceptable salt thereof in preparation of medicine for treating psoriasis
Ensartinib is used to prepare drugs for the treatment of psoriasis. By taking ensartinib or its hydrochloride orally, it improves psoriatic skin lesions and reduces skin tissue inflammation, solving the problems of large side effects and high cost of existing treatments, and has significant therapeutic effects.
Patent Information
- Application Number
- CN202511402285.6
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2025-09-28
- Publication Date
- 2025-11-21
AI Technical Summary
Existing medications for treating psoriasis have significant side effects and are expensive; there are no reports of ensartinib being effective in treating psoriasis.
Ensartinib or its pharmaceutically acceptable salts are used to prepare medicines for the treatment of psoriasis, administered orally at doses of 50 mg to 200 mg per day, to improve psoriasis-like skin lesions and reduce inflammation of skin tissue.
Ensartinib significantly improves psoriatic skin lesions and reduces skin tissue inflammation, demonstrating significant efficacy and broad application prospects.
Smart Images
Figure CN120983439A_ABST
Abstract
Description
Technical Field
[0001] This invention relates to the field of novel uses of ensartinib, and more particularly to the use of ensartinib or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating psoriasis. Background Technology
[0002] Psoriasis is a chronic, relapsing, inflammatory skin disease with a global prevalence of approximately 2%-3%. Its pathogenesis involves abnormal proliferation of keratinocytes, immune system dysregulation (such as activation of the IL-17 / 23 pathway), and angiogenesis.
[0003] Currently, clinical treatment options are limited. For mild cases, topical corticosteroids and vitamin D3 derivatives (such as calcipotriol) are used, but long-term use can lead to skin atrophy or drug resistance. For moderate cases, medications such as methotrexate and cyclosporine or biological inhibitors, such as TNF-α inhibitors, are used, but these carry risks of liver toxicity, infection, or high costs, with the annual cost of biological agents exceeding 100,000 yuan.
[0004] Ensartinib is a targeted therapy drug, belonging to the ALK tyrosine kinase inhibitor class, primarily used to treat ALK-positive locally advanced or metastatic non-small cell lung cancer (NSCLC). It controls cancer progression by inhibiting the abnormal activity of the ALK protein, blocking tumor growth signals. However, there are no reports on the use of ensartinib in treating psoriasis.
[0005] Therefore, in view of the above problems, the present invention urgently needs to provide the use of ensartinib or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating psoriasis. Summary of the Invention
[0006] The purpose of this invention is to provide the use of ensartinib or a pharmaceutically acceptable salt in the preparation of a medicament for treating psoriasis, thereby achieving the treatment of psoriasis with ensartinib.
[0007] This invention provides the use of ensartinib or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating psoriasis, wherein the structure of ensartinib is shown in Formula 1:
[0008]
[0009] Preferably, ensartinib or a pharmaceutically acceptable salt thereof is used to improve psoriatic skin lesions and reduce inflammation of skin tissue.
[0010] Preferably, ensartinib or a pharmaceutically acceptable salt thereof is administered to the subject in need at a dose of 50 mg to 200 mg / day, calculated as ensartinib.
[0011] Preferably, ensartinib or a pharmaceutically acceptable salt thereof is administered to the subject in need at a dose of 80-150 mg / day, calculated as ensartinib.
[0012] Preferably, ensartinib or a pharmaceutically acceptable salt thereof is administered to the subject in need at a dose of 100 mg per day, calculated as ensartinib.
[0013] Preferably, the pharmaceutically acceptable salt of ensartinib is one of the following: hydrochloride, phosphate, formate, acetate, maleate, or citrate.
[0014] Preferably, the pharmaceutically acceptable salt of ensartinib is the hydrochloride salt.
[0015] Preferably, the drug is one of an oral preparation, a tablet, or a capsule.
[0016] Preferably, when the drug is an oral preparation, the solvent is physiological saline.
[0017] The application of ensartinib or a pharmaceutically acceptable salt in the preparation of medicaments for treating psoriasis provided by this invention has the following advantages compared with the prior art:
[0018] This invention demonstrates, through studies on the effects of ensartinib (ESTN) on HaCaT cell viability, the effects of ensartinib on KGF-induced HaCaT cells, the effects of ensartinib on mouse skin damage, and the pathological changes in mice, that ensartinib has a significant therapeutic effect on psoriasis. At a certain dose, ensartinib does not affect HaCaT cell viability, and at the same time, it can significantly increase the levels of IL-17, IL-23, IL-6, and TNF-α.
[0019] This invention provides a new use for ensartinib, offering a novel drug for the treatment of psoriasis. Ensartinib can be taken orally to improve psoriasis-like skin lesions and reduce skin tissue inflammation, demonstrating significant efficacy in the treatment of psoriasis. It has broad application prospects and considerable value for widespread application. Attached Figure Description
[0020] To more clearly illustrate the specific embodiments of the present invention or the technical solutions in the prior art, the drawings used in the description of the specific embodiments or the prior art will be briefly introduced below. Obviously, the drawings described below are some embodiments of the present invention. For those skilled in the art, other drawings can be obtained from these drawings without creative effort.
[0021] Figure 1 This is a graph showing the effect of different concentrations of ensartinib on the viability of HaCaT cells.
[0022] Figure 2To illustrate the effect of ensartinib on KGF-induced HaCaT cells, (a) shows the cell viability test results, (b) shows the IL-17 level test results, (c) shows the IL-23 level test results, and (d) shows the cell viability test results.
[0023] IL-6 level test results, (e) is the TNF-α level test result;
[0024] Figure 3 To monitor skin damage during the modeling process of this invention, (a) shows the skin observation images of the backs of mice in each group, and (b) shows the PASI scores of the skin on the backs of mice in each group.
[0025] Figure 4 The images show the pathological changes in mice. (a) shows the observation of the stratum corneum of the mouse epidermis in each group, and (b) shows the results of the changes in the thickness of the mouse epidermis in each group. Detailed Implementation
[0026] The technical solution of the present invention will now be clearly and completely described with reference to the accompanying drawings. Obviously, the described embodiments are only some, not all, of the embodiments of the present invention. Based on the embodiments of the present invention, all other embodiments obtained by those skilled in the art without creative effort are within the scope of protection of the present invention.
[0027] This embodiment provides the use of ensartinib or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating psoriasis, wherein the structure of ensartinib is shown in Formula 1:
[0028]
[0029] Specifically, ensartinib or its pharmaceutically acceptable salts are used to improve psoriatic skin lesions and reduce inflammation of skin tissue.
[0030] Specifically, ensartinib or its pharmaceutically acceptable salts are administered to those in need, at a dose of 50-200 mg / day, calculated as ensartinib.
[0031] Specifically, ensartinib or its pharmaceutically acceptable salts are administered to those in need at a dose of 80-150 mg / day, calculated as ensartinib.
[0032] Specifically, ensartinib or its pharmaceutically acceptable salts are administered to the recipients in need at a dose of 100 mg per day, calculated as ensartinib.
[0033] Specifically, pharmaceutically acceptable salts of ensartinib are one of the following: hydrochloride, phosphate, formate, acetate, maleate, or citrate.
[0034] Specifically, the pharmaceutically acceptable salt of ensartinib is its hydrochloride salt.
[0035] Specifically, the drug is one of an oral dosage form, a tablet, or a capsule.
[0036] Specifically, when the drug is taken orally, the solvent is physiological saline.
[0037] Specifically, tablets can be produced by compression or molding.
[0038] Example 1
[0039] Effects of different concentrations of ensartinib (ESTN) on HaCaT cell viability.
[0040] 1) Experimental materials
[0041] Fetal bovine serum (S9020) (Solarbio, Beijing, China);
[0042] DMEM medium (11965092) (GIBCO, Invitrogen Corporation, NY, USA);
[0043] Penicillin-Streptomycin (15140148);
[0044] Trypsin (15140148) (Thermo Fisher Scientific, Pittsburgh, PA, USA); CCK-8 kit (C0037) (Beyotime, Shanghai, China);
[0045] Ensartinib is ensartinib hydrochloride;
[0046] HaCaT immortalized human epidermal cells were purchased from the China Center for Type Culture Collection (Hubei, China).
[0047] 2) CCK8 reagent kit detection method:
[0048] The specific steps are as follows: Centrifuge to collect cells incubated with different concentrations of ensartinib, and then... 4 The cells were seeded at a density of 1 / 2 wells into 96-well plates, with 3 replicates per group. The appropriate culture medium was added according to the grouping. After incubation, CCK-8 was used for measurement. The old culture medium was aspirated, and the cells were washed 3 times with PBS buffer. 100 μL of culture medium containing 10% CCK-8 working solution was added to each well, and the cells were gently shaken to mix. The cells were then placed in a cell culture incubator for incubation. After 2 hours of incubation, the absorbance values of each cell were measured at a wavelength of 450 nm using a microplate reader, and the results were compared and analyzed.
[0049] 3) Specific testing process for the effect on HaCaT cell viability: 301) HaCaT cell passage culture
[0050] Prepare a complete culture medium, which is DMEM medium containing penicillin (final concentration 100 U / mL), streptomycin (final concentration 100 μg / mL), and 10% fetal bovine serum. Add HaCaT cells to the DMEM medium. When the HaCaT cells reach 90% confluence, discard the old medium and wash the HaCaT cells twice with 2 mL of PBS buffer. Discard the PBS buffer and add 2 mL of 0.25% trypsin-0.02% EDTA digestion solution. Observe under a microscope for about 30 seconds. When the cells become rounded, quickly add 2 mL of complete medium to stop the digestion. Gently pipette and collect the cells. Centrifuge at 800 rpm, 4℃ for 5 min, discard the supernatant, resuspend the HaCaT cells in complete medium, and culture in separate flasks. Change the medium every other day.
[0051] 302) Prepare ensartinib at different concentrations, namely 0.1 nM, 10 nM, 100 nM, 500 nM, 1 μM, and 10 μM.
[0052] 303) The cultured HaCaT cells were added to different concentrations of ensartinib and incubated for 24 hours. After incubation, the cell viability of each group was detected by the CCK8 kit.
[0053] like Figure 1 As shown, HaCaT cells were incubated with different concentrations of ensartinib for 24 hours, and the cell survival rate of each group was observed.
[0054] The results of the three individual experiments in this embodiment are mean ± standard deviation, *P<0.05, **P<0.01.
[0055] from Figure 1 Observations revealed that, compared with the control group with an ensartinib concentration of 0, there were no significant changes in cell viability in the 1 nM, 10 nM, 100 nM, 500 nM, and 1 μM ensartinib groups, while cell viability was significantly decreased in the 10 μM ensartinib group.
[0056] Example 2
[0057] Effects of ensartinib on keratinocyte growth factor (KGF)-induced HaCaT cells 1) Experimental materials
[0058] Human IL-17Quantikine QuicKit ELISA(QK317);
[0059] Human IL-23Quantikine ELISA Kit(D2300B);
[0060] Human IL-6Quantikine QuicKit ELISA(QK206);
[0061] Human TNF-alpha Quantikine ELISA Kit (DTA00D) (R&D Systems, Minneapolis, USA);
[0062] Keratinocyte growth factor (KGF),
[0063] CCK-8 Reagent Kit (C0037) (Beyotime, Shanghai, China).
[0064] HaCaT immortalized human epidermal cells were purchased from the China Center for Type Culture Collection (Hubei, China).
[0065] 2) Testing Methods
[0066] 201) ELISA method for detecting IL-17 levels in supernatant
[0067] The specific steps are as follows:
[0068] A) Prepare the standards according to the reagent instructions. The concentrations of the IL-17A standards are as follows: 2000, 1000, 500, 250, 125, 62.5, 31.3, 0 pg / mL.
[0069] B) Remove excess microporous strips from the plate frame, put them back into the foil bag containing the desiccant, and reseal them;
[0070] C) Add 50 μL of standard, reference, or sample to each well;
[0071] D) Add 50 μL of antibody mixture to each well, seal with sealing film, and incubate at room temperature at 500 rpm for 1 hour;
[0072] E) Aspirate and wash each well, repeating this process twice for a total of three washes;
[0073] F) Add 100 μL of substrate solution to each well. Seal the plate with a new sealing membrane and incubate for 20 minutes.
[0074] G) Add 50 μL of stop solution to each well. Gently tap the plate to ensure thorough mixing;
[0075] H) The OD value was measured at 450 nm.
[0076] 202) ELISA assay method for detecting IL-23 levels in supernatant
[0077] The specific steps are as follows:
[0078] A) Prepare the standards according to the reagent instructions. The concentrations of the IL-23 standards are as follows: 2500, 1250, 625, 313, 156, 78.1, 39.1, 0 pg / mL.
[0079] B) Remove excess microporous strips from the plate frame, put them back into the foil bag containing the desiccant, and reseal them;
[0080] C) Add 100 μL of detection diluent RD1-22 to each well;
[0081] D) Add 100 μL of standard, control, or sample to each well. Seal the plate with sealing film and incubate at room temperature for 2 hours at 500 rpm.
[0082] E) Aspirate and wash each well, repeating this process 3 times for a total of 4 washes;
[0083] F) Add 200 μL of human IL-23 conjugate to each well. Seal the plate with a new sealing membrane. Incubate on a shaker at room temperature for 2 hours.
[0084] G) Repeat step 5;
[0085] H) Add 200 μL of substrate solution to each well. Incubate at room temperature in the dark for 30 minutes.
[0086] I) Add 50 μL of stop solution to each well. Gently tap the plate to ensure thorough mixing.
[0087] G) The OD value was measured at 450 nm.
[0088] 203) ELISA method for detecting IL-6 levels in supernatant
[0089] The specific steps are as follows:
[0090] A) Prepare the standards according to the reagent instructions. The concentrations of the IL-6 standards are as follows: 800, 400, 200, 100, 50, 25, 12.5, 0 pg / mL.
[0091] B) Remove excess microporous strips from the plate frame, put them back into the foil bag containing the desiccant, and reseal them;
[0092] C) Add 50 μL of detection diluent RD1-14 to each well;
[0093] D) Add 50 μL of standard, reference, or sample to each well. Seal the plate with sealing film and incubate at room temperature for 500 rpm.
[0094] E) Aspirate and wash each well, repeating this process twice for a total of three washes;
[0095] F) Add 100 μL of substrate solution to each well; seal the plate with a new sealing membrane and incubate for 20 minutes.
[0096] G) Add 50 μL of stop solution to each well. Gently tap the plate to ensure thorough mixing;
[0097] H) The OD value was measured at 450 nm.
[0098] 204) ELISA method for detecting TNF-α levels in supernatant
[0099] The specific steps are as follows:
[0100] A) Prepare the standards according to the reagent instructions. The concentrations of the TNF-α standards are as follows: 1000, 500, 250, 125, 62.5, 31.3, 15.6, 0 pg / mL.
[0101] B) Remove excess microporous strips from the plate frame, put them back into the foil bag containing the desiccant, and reseal them;
[0102] C) Add 50 μL of detection diluent RD1F to each well;
[0103] D) Add 50 μL of standard, control, or sample to each well. Seal the plate with sealing film and incubate at room temperature for 2 hours at 500 rpm.
[0104] E) Aspirate and wash each well, repeating this process 3 times for a total of 4 washes;
[0105] F) Add 200 μL of human TNF-α conjugate to each well. Seal the plate with a new sealing membrane. Incubate at room temperature for 2 hours;
[0106] G) Repeat step 5;
[0107] H) Add 200 μL of substrate solution to each well. Incubate at room temperature in the dark for 30 minutes.
[0108] I) Add 50 μL of stop solution to each well. Gently tap the plate to ensure thorough mixing;
[0109] G) The OD value was measured at 450 nm.
[0110] 3) Testing procedure for the effect of keratinocyte growth factor (KGF) induced in HaCaT cells: 301) Grouping:
[0111] Control group: HaCaT cells were cultured normally for 24 hours.
[0112] Model group (KGF): HaCaT cells were incubated with KGF-containing medium for 24 hours, with a final KGF concentration of 40 ng / mL.
[0113] 500nM ESTN group: HaCaT cells were incubated with KGF-containing medium for 24 hours, and then ensartinib was added for another 24 hours. The final concentration of KGF was 40ng / mL, and the final concentration of ESTN was 500nM.
[0114] 1μM ESTN group: HaCaT cells were incubated with KGF in a medium for 24 hours, and then ESTN was added for another 24 hours. The final concentration of KGF was 40ng / mL and the final concentration of ESTN was 1μM.
[0115] 302) After incubation, cell viability in the blank group, model group, 500 nM ESTN group and 1 μM ESTN group was detected using the CCK8 kit (the detection process of the CCK8 kit is the same as in Example 1); the levels of IL-17, IL-23, IL-6 and TNF-α in the cell culture supernatant of each group were detected by ELISA.
[0116] The results of the three individual experiments in this embodiment are mean ± standard deviation. *P<0.05, **P<0.01.
[0117] like Figure 2 The results shown are the cell viability test results and the level test results of IL-17, IL-23, IL-6, and TNF-α in the blank group, model group, 500nM ESTN group and 1μM ESTN group.
[0118] from Figure 2 It was observed that, compared with the control group, the cell viability of HaCaT cells in the model group was significantly improved, and the levels of IL-17, IL-23, IL-6, and TNF-α in the culture supernatant were significantly increased. Compared with the model group, the cell viability of HaCaT cells and the levels of IL-17, IL-23, IL-6, and TNF-α in the culture supernatant of the 500 nM test drug ensartinib group were slightly decreased, but the differences were not statistically significant; the cell viability of HaCaT cells and the levels of IL-17, IL-23, IL-6, and TNF-α in the culture supernatant of the 1 μM test drug ESTN group were significantly decreased.
[0119] Example 3
[0120] Animal experiments, monitoring mouse skin damage during modeling
[0121] 1) Experimental materials:
[0122] The mice were SPF-grade male BALB / c mice, 8 weeks old, weighing 22±2g, provided by Changzhou Cavens Laboratory Animal Co., Ltd., Animal Production License No.: SCXK(Su)2021-0013, Laboratory Animal Use License No.: SYXK(Su)2021-0007, and were housed in an environment of 21℃-25℃ with free access to food and water.
[0123] HE dye solution (G1120) (KeyGEN Biotech, Nanjing, China).
[0124] 2) Animal model construction
[0125] BALB / c mice were housed in an SPF-grade animal facility under controlled conditions of 21℃-25℃, relative humidity of 40%-70%, with alternating light and dark cycles of 12 hours per day, and free access to food. After one week of acclimatization, the fur on a 2×3cm area of the mouse's back was shaved using electric clippers, and fine downy hairs were removed using a single-headed electric shaver. The shaved mice were left untreated for 3 days to allow for the elimination of any damage or impact on the back skin caused by shaving. Except for the normal control group, the remaining mice were given 62.5mg / mouse of 5% imiquimod cream, applied evenly to the bare area of the mouse's back for 7 consecutive days. The control group mice were given the same dose of petroleum jelly for 7 consecutive days. Newly grown fine downy hairs were removed using a single-headed electric shaver, ensuring that the bare area of the mouse's back remained hairless throughout the entire process.
[0126] Data were analyzed and plotted using Graphpad Prism 9 (Version 9.4.0), and processed and combined using Adobe Illustrator 2022 (Version 2022). All data are expressed as mean ± SD. Statistical differences between groups were analyzed using one-way ANOVA and Tukey's test, with a p-value less than 0.05 considered statistically significant.
[0127] 3) HE staining method:
[0128] A) Baking: Place the prepared paraffin sections of skin tissue in an electric constant temperature drying oven and bake at 60℃ for 3 hours;
[0129] B) Dewax the dried paraffin sections using standard xylene, hydrate them with descending gradient ethanol, and wash them with distilled water; C) Stain the nuclei with hematoxylin for 2 min, differentiate them with hydrochloric acid alcohol for a few seconds, and wash them with water to restore their blue color.
[0130] D) Stain the slide with eosin solution for 1 minute, then rinse with water to remove any residual dye.
[0131] E) Sections were dehydrated and dried with a gradient of alcohols, cleared with xylene, and mounted with neutral resin;
[0132] F) Take pictures under a phase contrast microscope at 100× magnification. Use ImageJ to randomly measure the vertical distance from the stratum corneum to the basal layer of the epidermis at 3 locations and take the average to analyze the epidermal thickening.
[0133] 4) Specific experimental procedure
[0134] Group 401:
[0135] Control group: Mice were shaved on the back and then coated with an equal amount of petroleum jelly for 7 consecutive days. At the same time, they were given 0.1 ml / 10 g saline by gavage once a day for 7 consecutive days.
[0136] Model group: After shaving the back of mice, 5% imiquimod cream (dosage dose of 62.5mg / mouse) was applied to establish the model for 7 consecutive days. At the same time as establishing the model, 0.1ml / 10g physiological saline was administered by gavage once a day for 7 consecutive days.
[0137] Positive group: After shaving the back of mice, 5% imiquimod cream (dosage dose of 62.5 mg / mouse) was applied to establish the model for 7 consecutive days. At the same time as establishing the model, 5 mg / kg dexamethasone aqueous solution was administered by gavage once a day for 7 consecutive days.
[0138] ESTN-25mg / kg group: After shaving the back of mice, 5% imiquimod cream (dosage dose of 62.5mg / mouse) was applied to establish the model for 7 consecutive days; at the same time as establishing the model, ESTN 25mg / kg was administered by gavage once a day for 7 consecutive days.
[0139] ESTN-50mg / kg group: After shaving the back of mice, 5% imiquimod cream (dosage dose of 62.5mg / mouse) was applied to establish the model for 7 consecutive days; at the same time as establishing the model, 50mg / kg of the test drug ESTN was administered by gavage once a day for 7 consecutive days.
[0140] 402) Observe the skin lesions on the back of mice against a clean background at the same time every day and take pictures to record the changes in the skin lesions. Use the Psoriasis Skin Lesion Area and Severity (PASI) to score the skin lesions. Score independently according to the degree of erythema, scaling and thickening of the skin lesions of mice. Add the scores of the three to get the total score.
[0141] The PASI scoring criteria are as follows: None = 0 points; Mild = 1 point; Moderate = 2 points; Severe = 3 points; Very Severe = 4 points; Total score = scaling + thickening + erythema (0-12 points).
[0142] 403) HE staining detection: Mice were euthanized on day 8, and 0.5×1cm back skin lesions from each group of mice were taken for HE staining to observe and analyze the epidermal thickening.
[0143] like Figure 3 The image shows the observation of the skin on the back of the mouse and the PASI score; as shown. Figure 4 The image shows the condition of epidermal thickening.
[0144] from Figure 3 In the study, compared with the control group, the model group mice showed obvious erythema, scaling, and thickened skin on their backs, exhibiting psoriasis-like lesions, and their PASI scores were significantly higher. Compared with the model group, the positive control group and the ETSN-50 mg / kg group mice showed significant improvement in their back skin condition and significantly lower PASI scores; the ETSN-25 mg / kg group mice showed no significant change in their back skin PASI scores, indicating that ensartinib can improve psoriasis-like skin lesions.
[0145] from Figure 4 It was observed that the epidermis on the backs of mice in the control group was thinner, and the cells in the granular layer, spinous layer, and basal layer all exhibited normal structure and morphology. Compared with the control group, the dorsal skin tissue structure of mice in the model group was disordered, and the epidermal thickness was significantly increased. Compared with the model group, the epidermal thickness on the backs of mice in the positive control group and the ETSN-50mg / kg group was significantly reduced; the epidermal thickness on the backs of mice in the ETSN-25mg / kg group was slightly reduced, but not significantly.
[0146] Experimental results showed that ensartinib can improve psoriatic skin lesions and reduce skin tissue inflammation.
[0147] Finally, it should be noted that the above embodiments are only used to illustrate the technical solutions of the present invention, and not to limit them. Although the present invention has been described in detail with reference to the foregoing embodiments, those skilled in the art should understand that modifications can still be made to the technical solutions described in the foregoing embodiments, or equivalent substitutions can be made to some or all of the technical features therein. Such modifications or substitutions do not cause the essence of the corresponding technical solutions to deviate from the scope of the technical solutions of the embodiments of the present invention.
Claims
1. The use of ensartinib or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating psoriasis, characterized in that: The structure of ensartinib is shown in Formula 1:
2. The use of ensartinib or a pharmaceutically acceptable salt thereof according to claim 1 in the preparation of a medicament for treating psoriasis, characterized in that: Ensartinib or its pharmaceutically acceptable salts are used to improve psoriatic skin lesions and reduce inflammation of skin tissues.
3. The use of ensartinib or a pharmaceutically acceptable salt thereof according to claim 1 in the preparation of a medicament for treating psoriasis, characterized in that: Administer ensartinib or its pharmaceutically acceptable salt to those in need at a dose of 50-200 mg / day, based on ensartinib.
4. The use of ensartinib or a pharmaceutically acceptable salt thereof according to claim 3 in the preparation of a medicament for treating psoriasis, characterized in that: Administer ensartinib or its pharmaceutically acceptable salt to those in need at a dose of 80-150 mg / day, based on ensartinib.
5. The use of ensartinib or a pharmaceutically acceptable salt thereof according to claim 4 in the preparation of a medicament for treating psoriasis, characterized in that: Administer ensartinib or its pharmaceutically acceptable salt to the recipient in need at a dose of 100 mg per day, based on ensartinib.
6. The use of ensartinib or a pharmaceutically acceptable salt thereof according to claim 1 in the preparation of a medicament for treating psoriasis, characterized in that: Pharmaceutically acceptable salts of ensartinib are one of the following: hydrochloride, phosphate, formate, acetate, maleate, or citrate.
7. The use of ensartinib or a pharmaceutically acceptable salt thereof according to claim 1 in the preparation of a medicament for treating psoriasis, characterized in that: The pharmaceutically acceptable salt of ensartinib is its hydrochloride salt.
8. The use of ensartinib or a pharmaceutically acceptable salt thereof according to claim 1 in the preparation of a medicament for treating psoriasis, characterized in that: The drug is one of the following: oral dosage form, tablet, or capsule.
9. The use of ensartinib or a pharmaceutically acceptable salt according to claim 8 in the preparation of a medicament for treating psoriasis, characterized in that: When the drug is taken orally, the solvent is physiological saline.