A small molecule inhibitor targeting the fc epsilon ri gamma subunit and uses thereof

Abstract

This invention provides a small molecule inhibitor targeting the FcεRIγ subunit and its application. It discovers that erythrophenol can act as a small molecule inhibitor targeting the FcεRIγ subunit, thereby inhibiting the occurrence of allergic reactions. This invention confirms the direct binding interaction between erythrophenol and the FcεRIγ subunit using SPR and CETSA techniques, revealing that erythrophenol can target and inhibit the FcεRIγ subunit. Furthermore, this invention finds that erythrophenol can significantly inhibit the release of IgE signal-induced β-aminoglycosidase in mast cells, exhibiting a significant ability to inhibit IgE signal-mediated mast cell degranulation and suppress mast cell activation-mediated allergic reactions. This fully demonstrates that erythrophenol, as an inhibitor targeting the FcεRIγ subunit, holds promise as the first inhibitor to induce FcεRIγ subunit degradation in anti-type I allergic diseases, and has broad application prospects for further use in anti-allergy treatment.

Description

Technical Field

[0001] This invention relates to the field of biomedicine, and in particular to a small molecule inhibitor that targets and inhibits the FcεRIγ subunit and its application. Background Technology

[0002] Allergic reactions, also known as hypersensitivity reactions, are a group of diseases caused by the re-stimulation of an already sensitized body by allergens, resulting in hypersensitivity or abnormal immune function. They typically cause tissue damage or functional disorders, and in severe cases, can even threaten life and health. Allergic reactions caused by allergens entering the body can be localized or systemic; systemic allergies can lead to shock and even death. In recent years, the incidence of allergic diseases has continued to rise, seriously affecting human quality of life and global public health.

[0003] Mast cells, as the primary target cells in the immediate phase of type I hypersensitivity reactions, play a crucial role in allergic and inflammatory responses, mainly due to the high expression of high affinity IgE receptors (FcεRI) on their surface. During a type I hypersensitivity reaction, the high affinity IgE receptors on the mast cell surface bind to IgE antibody / antigen complexes in serum, prompting the release of granules, inflammatory mediators, and cellular inflammatory factors. Free IgE molecules in serum bind to FcεRI receptor molecules on the mast cell surface, inducing an allergic reaction in the body. The sensitized state typically lasts for months or even longer, gradually disappearing if there is prolonged avoidance of the same allergen. However, once an allergen binds to specific IgE antibodies bound to FcεRI on the mast cell surface, it rapidly causes FcεRI cross-linking, prompting the release of granules and inflammatory mediators and cellular inflammatory factors within the granules, leading to immediate-type allergic reaction symptoms within the tissue. Therefore, targeting and inhibiting mast cell activation is one of the main directions in the development of anti-allergy drugs.

[0004] Methods to interfere with and block IgE-FcεRI signal transduction include preventing IgE from binding to the FcεRI receptor and inhibiting signal amplification and transduction. The cross-linking of allergens with specific IgE and their subsequent binding to FcεRI on the mast cell surface to initiate transmembrane signal transduction is a key step in the development of inflammatory symptoms in type I hypersensitivity reactions. The FcεRI receptor heteropolymer complex, a multi-chain immune recognition receptor, exists on the target cell membrane in the form of αβγ2 tetramers or αγ2 trimers. The tetrameric FcεRI is mainly expressed on the surface of mast cells and basophils, mediating type I hypersensitivity reactions. The FcεRI α subunit determines the initiation of the IgE / FcεRI cross-linking signal; the FcεRI β subunit with an ITAM (Immunoreceptor tyrosine-based activation motif, ITAM) structure amplifies the signal transduction process; and the FcεRI γ subunit, also possessing an ITAM structure, plays a crucial role in downstream signal transduction. The FcεRIγ chain, encoded by the Fcer1g gene, is a disulfide-linked γ2 homodimer, with each γ chain containing an ITAM activation motif. FcεRIγ and its ITAM are crucial for downstream signal transduction of the IgE / FcεRI cross-linked complex. Knock-Out mouse studies have shown that FcεRIγ gene deletion prevents IgE from inducing mast cell activation and hypersensitivity responses. Therefore, small-molecule inhibitors that target and degrade FcεRIγ to block its signal transduction could be an innovative approach for developing treatments for type I hypersensitivity diseases.

[0005] However, no lead compounds targeting and inhibiting the FcεRIγ subunit have been reported to date. Therefore, the existing technology still needs improvement and development. Summary of the Invention

[0006] In view of the shortcomings of the prior art, the purpose of this invention is to provide a small molecule inhibitor that targets and inhibits the FcεRIγ subunit and its application, aiming to solve the problem of the lack of lead compounds that target and inhibit the FcεRIγ subunit in the prior art.

[0007] The technical solution of the present invention is as follows:

[0008] A small molecule inhibitor targeting and inhibiting the FcεRIγ subunit, wherein the small molecule inhibitor comprises erythrophenol; the structural formula of erythrophenol is as follows:

[0009]

[0010] The small molecule inhibitor that targets and inhibits the FcεRIγ subunit, wherein the red phenol achieves the effect of targeting and inhibiting the FcεRIγ subunit by directly binding to it.

[0011] The small molecule inhibitor that targets and inhibits the FcεRIγ subunit comprises, wherein the red phenol forms three hydrogen bonds and a hydrophobic interaction with the FcεRIγ protein to achieve the effect of targeting and inhibiting the FcεRIγ subunit; wherein the phenolic hydroxyl group of the red phenol acts as a hydrogen bond donor to form three hydrogen bonds with the amino acid residues Glu59 and Thr66 of the FcεRIγ subunit, and the distances between the hydrogen bonds and the paired atoms are respectively... The red phenol forms a hydrophobic interaction with the amino acid residues Lys60, Asp62, and Gly63 of the FcεRIγ subunit.

[0012] The small molecule inhibitor that targets and inhibits the FcεRIγ subunit, wherein the red betaine inhibits IgE signaling-mediated allergic reactions by targeting and inhibiting the FcεRIγ subunit.

[0013] The small molecule inhibitor that targets and inhibits the FcεRIγ subunit, wherein the red betaine inhibits the release of β-aminoglycosidase in mast cells mediated by IgE signaling, thereby inhibiting the degranulation ability of mast cells and achieving the effect of inhibiting type I hypersensitivity reaction.

[0014] Application of a small molecule inhibitor that targets and inhibits the FcεRI γ subunit in the study of the molecular mechanism of IgE-FcεRI crosslinking signal transduction, wherein the small molecule inhibitor contains rubigin.

[0015] The application of a small molecule inhibitor that targets and inhibits the FcεRIγ subunit in the preparation of an anti-allergy drug, wherein the small molecule inhibitor comprises rubiphenol.

[0016] The application of a small molecule inhibitor that targets and inhibits the FcεRIγ subunit in the preparation of an inhibitor for type I allergic diseases, wherein the small molecule inhibitor comprises rubeophenol.

[0017] Application of a small molecule inhibitor targeting the FcεRIγ subunit in screening drug targets for allergic reactions, wherein the small molecule inhibitor comprises rubigin.

[0018] A kit for targeting and inhibiting the FcεRIγ subunit, wherein the kit comprises a small molecule inhibitor targeting and inhibiting the FcεRIγ subunit as described above.

[0019] Beneficial Effects: This invention provides a small molecule inhibitor targeting the FcεRIγ subunit and its application. It discovers that erythropoietin can act as a small molecule inhibitor targeting the FcεRIγ subunit, thereby inhibiting the occurrence of allergic reactions. This invention confirms the direct binding interaction between erythropoietin and the FcεRIγ subunit using SPR and CETSA techniques, revealing that erythropoietin can target and inhibit the FcεRIγ subunit. Furthermore, this invention finds that erythropoietin can significantly inhibit the release of IgE-induced β-aminoglycosidase in mast cells, exhibiting a significant ability to inhibit IgE-mediated mast cell degranulation and suppress mast cell activation-mediated allergic reactions. This fully demonstrates that erythropoietin, as an inhibitor targeting the FcεRIγ subunit, holds promise as the first inhibitor to induce FcεRIγ subunit degradation in anti-type I allergic diseases, and has broad application prospects for further use in anti-allergy treatment. Attached Figure Description

[0020] Figure 1 This is a schematic diagram of the 3D simulation structure of PPG and FcεRIγ molecular docking provided in an embodiment of the present invention.

[0021] Figure 2 This is a schematic diagram illustrating the direct binding interaction between PPG and FcεRIγ protein, provided in an embodiment of the present invention.

[0022] Figure 3 This is a schematic diagram showing the results of PPG inhibiting FcεRIγ protein expression in an embodiment of the present invention.

[0023] Figure 4 This is a schematic diagram showing the results of PPG inhibiting the degranulation and histamine production of RBL-2H3 according to an embodiment of the present invention.

[0024] Figure 5 This is a schematic diagram of the PPG-inhibited PCA model provided in an embodiment of the present invention.

[0025] Figure 6 This is a schematic diagram of the PPG-inhibited ASA model provided in an embodiment of the present invention. Detailed Implementation

[0026] This invention provides a small molecule inhibitor that targets and inhibits the FcεRIγ subunit and its application. To make the objectives, technical solutions, and effects of this invention clearer and more explicit, the invention is further described in detail below. It should be understood that the specific embodiments described herein are merely illustrative of the invention and are not intended to limit the invention.

[0027] This invention provides a small molecule inhibitor that targets and inhibits the FcεRIγ subunit, wherein the small molecule inhibitor comprises erythrophenol; the structural formula of erythrophenol is as follows:

[0028]

[0029] Currently, small molecule inhibitors that target and degrade FcεRIγ, blocking its signal transduction, have become an innovative approach for developing treatments for type I hypersensitivity diseases. Virtual screening based on drug libraries has emerged as one solution. Virtual screening is a drug library screening based on small molecule databases. Utilizing molecular docking operations between small molecule compounds and drug targets, virtual screening can rapidly identify druggable active compounds from millions of molecules. Its advantages include reducing the number of real compounds required for experimental screening and lowering drug development costs. The positive rate of this high-throughput screening is 5%-30%. Due to its speed, efficiency, and low cost, there are increasing reports of successfully obtaining therapeutic drugs or lead compounds through virtual screening.

[0030] This invention, based on the principle of "drug repurposing," applies this technology to screen lead compounds that target and inhibit the FcεRIγ subunit of mast cells. Through multiple rounds of screening from 500,000 compounds, this invention identified potential candidate compounds and, combined with in vitro pharmacodynamic screening, selected Purpurogallin (PPG), a small molecule compound that is effective, readily available, and has low toxicity in targeting and inhibiting the FcεRIγ subunit. Purpurogallin (PPG), also known as red phenol, is a natural phenol extracted from oak plants. It possesses strong xanthine oxidase inhibitory activity and also exhibits antioxidant and anti-inflammatory effects. This invention demonstrates that Purpurogallin can target and inhibit the FcεRIγ subunit, thereby suppressing allergic reactions.

[0031] In some embodiments, the erythrophenol achieves targeted inhibition of the FcεRIγ subunit by directly binding to it.

[0032] In some embodiments, the erythrophenol forms three hydrogen bonds and a hydrophobic interaction with the FcεRIγ protein, achieving targeted inhibition of the FcεRIγ subunit; wherein, the phenolic hydroxyl group of the erythrophenol acts as a hydrogen bond donor, forming three hydrogen bonds with the amino acid residues Glu59 and Thr66 of the FcεRIγ subunit, and the distances between the hydrogen bonds and the paired atoms are respectively... The red phenol forms a hydrophobic interaction with the amino acid residues Lys60, Asp62, and Gly63 of the FcεRIγ subunit.

[0033] This invention discloses a small molecule compound, rubigin, with significant efficacy and no obvious cytotoxicity, obtained through high-throughput drug screening. The direct binding interaction between rubigin and the FcεRIγ subunit was confirmed using SPR (surface plasmon resonance) and CETSA techniques. The 3D simulated structure of the docking between rubigin and the FcεRIγ molecule is shown below. Figure 1As shown. Red phenol can form three hydrogen bonds and hydrophobic interactions with human FcεRIγ protein: multiple phenolic hydroxyl groups act as hydrogen bond donors, forming three hydrogen bonds with Glu59 and Thr66, with distances of [missing information]. In addition, PPG can also form hydrophobic interactions with amino acid residues such as Lys60, Asp62, and Gly63.

[0034] In some embodiments, the erythrophenol can inhibit the expression of FcεRIγ protein.

[0035] In some embodiments, the erythromycin inhibits IgE signaling-mediated allergic reactions by targeting and inhibiting the FcεRIγ subunit.

[0036] In some embodiments, the red beta-phenol inhibits the release of β-aminoglycosidase from mast cells, thereby inhibiting the degranulation ability of mast cells and thus achieving the effect of inhibiting type I hypersensitivity reactions.

[0037] Allergic diseases have been listed by the World Health Organization (WHO) as one of the three major diseases requiring prevention and control in the 21st century, representing a significant global health problem. Mast cells are central to the initiation and maintenance of inflammation, playing a crucial role in type I hypersensitivity reactions. The IgE-FcεRIγ cross-linking signal is a key step in the initiation of type I hypersensitivity reactions. Therefore, targeting and inhibiting IgE-FcεRIγ cross-linking signal transduction is one of the important pathways to control mast cell-activated inflammation in type I hypersensitivity reactions. This invention discovers that erythromycin can inhibit the release of β-aminoglycosidase from mast cells, thereby inhibiting the degranulation ability of mast cells and achieving the effect of suppressing type I hypersensitivity reactions.

[0038] Specifically, the red beta-phenol inhibits the release of β-aminoglycosidase in mast cells RBL-2H3, thereby inhibiting the degranulation ability of mast cells RBL-2H3 and achieving the effect of inhibiting type I hypersensitivity reaction.

[0039] Rat basophils (RBL-2H3) exhibit a strong allergic immune response in the diagnosis and immunotherapy of allergies. RBL-2H3 cells possess high-affinity IgE receptors. Accumulation of these receptors or synergistic action with calcium ion carriers can activate their secretion of histamine and other neurotransmitters. This cell line is widely used to study mast cell FcERI and its secretory biochemical pathways. This invention reveals that PPG significantly inhibits RBL-2H3 degranulation.

[0040] This invention also provides the application of a small molecule inhibitor that targets and inhibits the FcεRIγ subunit in the preparation of anti-allergy drugs.

[0041] In some embodiments, the anti-allergy drug includes a pharmaceutically acceptable carrier or excipient.

[0042] In some embodiments, the anti-allergy drug includes tablets, capsules, injections, oral liquid preparations, and granules.

[0043] Red betaine is a known pharmaceutically active substance that can be prepared into any clinically applicable drug formulation using conventional methods, such as powders, tablets, microcapsules, capsules, microencapsulations, injections, granules, or liquids.

[0044] In the process of preparing the above-mentioned formulation, red betaine can be used alone or mixed with any excipient suitable for preparing a clinical drug to prepare a drug formulation.

[0045] This invention also provides an application of a small molecule inhibitor that targets and inhibits the FcεRI γ subunit in studying the molecular mechanism of IgE-FcεRI crosslinking signal transduction.

[0046] This invention also provides the application of a small molecule inhibitor that targets and inhibits the FcεRIγ subunit in the preparation of an inhibitor for type I allergic diseases.

[0047] This invention also provides an application of a small molecule inhibitor that targets and inhibits the FcεRIγ subunit in screening drug targets for allergic reactions.

[0048] Specifically, the small molecule inhibitors that target and inhibit the FcεRIγ subunit include erythrophenol.

[0049] More specifically, the erythrophenol can inhibit passive cutaneous anaphylaxis in mice.

[0050] Passive cutaneous anaphylaxis (PCA) in mice is associated with mast cell degranulation. Histamine released during mast cell degranulation increases vascular permeability, leading to Evans blue dye deposition and ear swelling. This invention demonstrates that PPG can significantly inhibit mast cell activation in mouse ear skin, and PPG can significantly reduce the degree of ear swelling and Evans blue accumulation in mice.

[0051] More specifically, the erythromycin can inhibit OVA-induced systemic allergic reactions in mice.

[0052] The OVA-induced systemic anaphylaxis model is a well-established model for studying anti-allergic drugs. Successful induction of an allergic reaction results in significant fluctuations in body temperature, and increases in histamine, cytokines IL-4, and IL-10. This invention demonstrates that PPG can significantly inhibit these fluctuations in body temperature.

[0053] This invention also provides a kit for targeting and inhibiting the FcεRIγ subunit, the kit comprising the above-mentioned small molecule inhibitors targeting and inhibiting the FcεRIγ subunit.

[0054] The following specific examples further illustrate the invention's small molecule inhibitor targeting the FcεRIγ subunit and its applications:

[0055] Unless otherwise specified, all reagents and materials used in the examples are commercially available.

[0056] Example 1: Determination of the direct binding interaction between PPG and FcεRIγ protein

[0057] SPR (surface plasmon resonance) technology can directly measure the in vitro interaction between FcεRIγ protein and PPG. This invention expresses recombinant FcεRIγ protein through genetic engineering and synthesizes various peptides using peptide synthesis methods for SPR analysis (Biacore T200, Cytiva).

[0058] The results are as follows Figure 2 As shown, the results indicate that PPG has a direct binding effect with FcεRIγ protein.

[0059] Example 2: PPG inhibits FcεRIγ protein expression

[0060] 1. Cell culture: BMMCs were isolated from Balb / c mice (purchased from Guangdong Provincial Medical Laboratory Animal Center) and cultured for 4-6 weeks in RPMI, 10% FBS, 1% penicillin antibody, 10 ng / ml IL-3 and SCF.

[0061] 2. Western Blotting: Add 10 μM and 20 μM PPG to BMMC cell suspension and incubate for 2 hours. Then, stimulate cells with DNP-HSA (DNP-conjugated human serum albumin) for 20 minutes. Discard the culture medium, add protein lysis buffer (containing protease inhibitors), and lyse on ice. Collect the supernatant protein. Quantify protein using the BCA method, following the BCA kit instructions. Prepare the required concentration of protein gel and perform SDS-PAGE. After blocking, incubate with the corresponding primary antibody overnight at 4°C. The next day, recover the primary antibody and wash the PVDF membrane three times with 1×TBST washing buffer for 8-10 minutes each time. Incubate with the corresponding secondary antibody on a shaker at room temperature, and then wash the membrane again using the same steps. After washing, prepare chemiluminescence buffer and develop / expose the membrane.

[0062] The results are as follows Figure 3 As shown, the results indicate that PPG can significantly inhibit the expression of FcεRIγ protein.

[0063] Example 3: Inhibitory effect of PPG on basophil degranulation

[0064] Rat basophils (RBL-2H3) exhibit a strong allergic immune response in the diagnosis and immunotherapy of allergies. RBL-2H3 cells possess high-affinity IgE receptors. Accumulation of these receptors or synergistic action with calcium ion carriers can activate their secretion of histamine and other neurotransmitters. This cell line is widely used to study mast cell FcERI and its secretory biochemical pathways. Specific implementation methods are as follows:

[0065] 1. Cell Culture: RBL-2H3 (purchased from Guangzhou Saiku Biotechnology Co., Ltd.) contains a high-affinity IgE receptor. After overnight incubation with 50 ng / ml anti-dinitrophenyl (DNP) IgE (sig), it was activated with DNP-HSA. RBL-2H3 was cultured in DMEM with 10% fetal bovine serum, 1% penicillin-antibody antibiotics, and 1% non-essential amino acids.

[0066] 2. CCK8 assay for the cytotoxic effect of PPG: RBL-2H3 (2×10⁻⁶) was used to detect the cytotoxic effect of PPG on cells. 3 Each well was seeded with PPG, and incubated for another 24 hours. Then, 10 μl of CCK8 reagent was added, and incubation was continued for 1 hour. Finally, the absorbance (OD value) was measured using a microplate reader at 450 nm. The results are as follows: Figure 4 As shown in Figure A.

[0067] 3. Release of β-hexosaminease: RBL-2H3 cells were seeded in 12-well plates and sensitized overnight with anti-DNP IgE, followed by PPG incubation for two hours. After drug incubation, the lysis group was lysed with Trixon at a final concentration of 0.1% for half an hour, while the model and experimental groups were stimulated with DNP-HSA (100 ng / mL) for half an hour (drug addition and concentration for each group are as follows). Figure 4 (As shown in Figure B). After stimulation with DNP-HSA for 30 min, 50 μl of supernatant was reacted with 50 μl of substrate at 37 °C for 90 min, and the absorbance was measured at 405 nm. The OD value of each group / OD value of the lysis group is the amount of β-hexosaminease released (expressed as a percentage), and the results are shown in Figure B. Figure 4 As shown in B.

[0068] 4. Measurement of histamine release: Mast cells sensitized overnight with anti-DNP-IgE were washed with PBS and incubated for 2 hours with different concentrations of PPG (10 μM and 20 μM) prepared with Timofe elixir. Then, DNP-HSA (100 ng / ml) diluted with the same Timofe elixir was added. The drug addition and concentration for each group are as follows: Figure 4As shown in Figure C, the cells were then placed in an incubator for stimulation for half an hour, and finally the cell supernatant was collected for histamine measurement. Histamine measurement was performed according to the histamine ELISA kit manufacturer's instructions. Results are as follows... Figure 4 As shown in C.

[0069] As shown in results 4A-C above, PPG can significantly inhibit the degranulation of RBL-2H3.

[0070] Example 4: Effects of PPG on passive cutaneous anaphylaxis in mice

[0071] Passive cutaneous anaphylaxis (PCA) in mice is associated with mast cell degranulation. Histamine released during mast cell degranulation increases vascular permeability, leading to Evans blue dye deposition and ear swelling. Experiments have shown that PPG significantly inhibits mast cell activation in mouse ear skin, reducing ear swelling and Evans blue accumulation in the experimental group. The specific implementation method is as follows:

[0072] 1. Feeding of BALB / c mice: Female BALB / c mice (4-5 weeks old) were purchased from Guangdong Provincial Medical Laboratory Animal Center (Foshan, Guangdong) and kept in a relatively stable SPF environment with temperature (24±1℃) and humidity (55±10%) for 1 week. Mice were used to isolate bone marrow-derived mast cells (BMMCs) and to establish passive cutaneous anaphylactic reaction (PCA) and active systemic anaphylactic reaction (ASA) models.

[0073] 2. Mouse treatment: Each mouse was injected with 0.5 μg of Anti-IgE into its ear and infiltrated for 24 hours before being injected intraperitoneally. One hour later, DNP-HSA and Evans blue were injected via the tail vein. One hour later, the mice were euthanized by cervical dislocation, and changes in ear color were observed. Mouse ears were extracted with formamide solution at 62℃ for 24 hours, and the OD value was measured at 620 nm. The thickness of the mouse ears was measured using a micrometer, and sections were stained with toluidine blue to observe changes in the number of activated mast cells.

[0074] The results are as follows Figure 5 As shown, Ketotifen is a histamine 1 (H1) receptor blocker and mast cell stabilizer. The figure shows that PPG significantly inhibited mast cell activation in the skin of mouse ears, reducing swelling and Evans blue accumulation in the experimental group mice.

[0075] Example 5: Effect of PPG on OVA-induced systemic allergic reactions

[0076] OVA-induced systemic anaphylaxis is a well-established model for studying anti-allergic drugs. Successful induction of the allergic reaction results in significant fluctuations in body temperature, and increases in histamine, cytokines IL-4, and IL-10. Compared to the control group, PPG significantly inhibited these temperature fluctuations.

[0077] Mouse treatment: On days 0 and 7, all mice except the control group (Ctrl) were sensitized by intraperitoneal injection of OVA diluted with aluminum adjuvant (200 μg). From days 9 to 13, the experimental group and the positive control group were intraperitoneally injected with PPG (15 mg / kg) and ketotifen (50 mg / kg), respectively, every other day. On day 14, sensitization was induced again by intraperitoneal injection of 200 μg of OVA and aluminum adjuvant. Rectal temperature was then measured every 10 minutes using a specific thermometer for a total of 9 rounds. After measurement, blood was collected from the orbital vein, and serum was obtained by centrifugation after the whole blood had been allowed to stand at room temperature for half an hour.

[0078] Detailed results are as follows Figure 6 As shown in the figure, PPG can significantly suppress fluctuations in body temperature.

[0079] In summary, this invention provides a small molecule inhibitor targeting the FcεRIγ subunit and its application. It discovers that erythrophenol can act as a small molecule inhibitor targeting the FcεRIγ subunit, thereby inhibiting the occurrence of allergic reactions. This invention confirms the direct binding interaction between erythrophenol and the FcεRIγ subunit using SPR and CETSA techniques, revealing that erythrophenol can target and inhibit the FcεRIγ subunit. Furthermore, this invention finds that erythrophenol can significantly inhibit the release of IgE signal-induced β-aminoglycosidase in mast cells, exhibiting a significant ability to inhibit IgE signal-mediated mast cell degranulation, and also inhibiting mast cell activation-mediated allergic reactions. This fully demonstrates that erythrophenol, as an inhibitor targeting the FcεRIγ subunit, holds promise as the first inhibitor to induce FcεRIγ subunit degradation in anti-type I allergic diseases, and has broad application prospects for further use in anti-allergy treatment.

[0080] It should be understood that the application of the present invention is not limited to the examples above. Those skilled in the art can make improvements or modifications based on the above description, and all such improvements and modifications should fall within the protection scope of the appended claims.

Claims

1. Use of a small molecule inhibitor targeting the FcεRIγ subunit in the manufacture of an anti-allergic medicament, characterized in that, The small molecule inhibitor is rhodotorulic acid, and the anti-allergic drug is an anti-type I allergy drug; the structural formula of the rhodotorulic acid is 。

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