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CN-122028926-A - Combined Chinese and Western medicine therapy for treating amyotrophic lateral sclerosis patient

CN122028926ACN 122028926 ACN122028926 ACN 122028926ACN-122028926-A

Abstract

Use of a component of a Traditional Chinese Medicine (TCM) for the manufacture of a medicament for reducing the effect of Amyotrophic Lateral Sclerosis (ALS) or neurodegeneration on a susceptible person, wherein the traditional Chinese medicine comprises (1) an extract of kudzuvine root, (2) angelica, (3) salvia miltiorrhiza, (4) codonopsis pilosula, (5) astragalus mongholicus, (6) perilla fruit, (7) jujube, (8) bupleurum, 9) scutellaria baicalensis, (10) safflower, (11) curcuma aromatica, (12) rheum officinale, (13) pricklyash, (14) liquorice, (15) ophiopogon root, (16) shizandra berry, (17) aconite, 18) ginseng, (19) poria cocos, (20) gypsum, (21) oyster, (22) cassia twig and (23) plantain seed, or the amount of the extract is equivalent to the amount of the raw materials of the corresponding components. The patent aims at clinical curative effects of amyotrophic lateral sclerosis diseases with different pathological manifestations. The medicine can be combined with western medicines.

Inventors

  • YANG XIONGZHE
  • LIU JIANBO
  • Chang Xiaoyue

Assignees

  • 协峰分子医疗有限公司

Dates

Publication Date
20260512
Application Date
20250320
Priority Date
20240719

Claims (10)

  1. 1. A method for reducing the effects of Amyotrophic Lateral Sclerosis (ALS) or neurodegeneration on a susceptible person, comprising administering to the susceptible person an effective amount of a Traditional Chinese Medicine (TCM) selected from the group consisting of: (1) radix Puerariae, (2) radix Angelicae sinensis, (3) radix Salviae Miltiorrhizae, (4) radix Codonopsis, (5) radix astragali, (6) fructus Perillae, (7) fructus Jujubae, (8) radix bupleuri, (9) radix Scutellariae, (10) flos Carthami, (11) radix Curcumae, (12) radix Et rhizoma Rhei, (13) fructus Zanthoxyli, (14) radix Glycyrrhizae, (15) radix Ophiopogonis, (16) fructus Schisandrae, (17) radix Aconiti lateralis Preparata, (18) radix Ginseng, (19) Poria, (20) Gypsum Fibrosum, (21) Concha Ostreae, (22) ramulus Cinnamomi, and (23) semen plantaginis, or An extract thereof in an amount corresponding to the amount of the raw materials of the corresponding ingredients of the set of ingredients.
  2. 2. The method of claim 1, wherein the effects of neurodegeneration in the subject are caused by Amyotrophic Lateral Sclerosis (ALS).
  3. 3. The method of claim 1, wherein the dosage form of the traditional Chinese medicine comprises decoction, granule, capsule, powder, water pill, tablet, mixture, oral liquid or other dosage forms.
  4. 4. The method of claim 1, wherein the traditional Chinese medicine is administered continuously to the susceptible person for at least 3 months to obtain an effective effect.
  5. 5. A method according to claim 1 or 4 wherein the traditional Chinese medicine is administered alone or in combination with a western medicine using a glutamate inhibitor, including but not limited to riluzole, edaravone or tofumet or other similar western medicine.
  6. 6. The method of claim 5, wherein the pharmaceutical agents used in the western medicine are used simultaneously, separately or sequentially to treat a susceptible individual.
  7. 7. Use of a traditional Chinese medicine for the manufacture of a formulation according to claim 3 for the treatment of neurodegenerative diseases, including but not limited to for repairing cell damage and promoting muscle healing.
  8. 8. A Chinese medicinal product comprises radix astragali 10-15 weight parts, radix Puerariae 5-10 weight parts, radix Angelicae sinensis 3-6 weight parts, carthami flos 1.5-3 weight parts, saviae Miltiorrhizae radix 3-6 weight parts, radix Curcumae 1.5-3 weight parts, radix et rhizoma Rhei 1-2 weight parts, bupleuri radix 1.5-3 weight parts, scutellariae radix 1.5-3 weight parts, fructus Perillae 3-6 weight parts, radix Codonopsis 3-6 weight parts, fructus Zanthoxyli 1-2 weight parts, glycyrrhrizae radix 1-2 weight parts and fructus Jujubae 1.5-3 weight parts.
  9. 9. A Chinese medicinal product comprises Ginseng radix 1-2 weight parts, radix Aconiti lateralis Preparata 1.5-3 weight parts, poria 1.5-3 weight parts, radix Ophiopogonis 3-6 weight parts, fructus Schisandrae 1.5-3 weight parts, and radix astragali 6-10 weight parts.
  10. 10. A Chinese medicinal product comprises Gypsum Fibrosum 3-6 weight parts, ramulus Cinnamomi 1-2 weight parts, concha Ostreae 3-6 weight parts, semen plantaginis 1-2 weight parts, bupleuri radix 1.5-3 weight parts, scutellariae radix 1.5-3 weight parts, fructus Perillae 3-6 weight parts, radix Codonopsis 3-6 weight parts, fructus Zanthoxyli 1-2 weight parts, glycyrrhrizae radix 1-2 weight parts and fructus Jujubae 1.5-3 weight parts.

Description

Combined Chinese and Western medicine therapy for treating amyotrophic lateral sclerosis patient Technical Field The invention relates to a method for treating amyotrophic lateral sclerosis (Amyotrophic Lateral Sclerosis, ALS) patients by utilizing the combination of traditional Chinese medicine and modern western medicine or not. Background Neurodegeneration refers to the progressive and irreversible loss of neuronal structure or function, neurons being specialized cells in the brain and spinal cord that transmit nerve impulses. Amyotrophic Lateral Sclerosis (ALS) is considered a neurodegenerative disease caused by loss of motor neurons. Because the biological processes that induce amyotrophic lateral sclerosis and drive disease progression are not well understood, there is a lack of effective treatments. The early stages of amyotrophic lateral sclerosis are mainly manifested by amyotrophy and weakness of the extremities. Advanced stages may incorporate bulbar paralysis, resulting in dysarthria, dysphagia, and dyspnea. Examination of the nervous system shows that tendon reflex is active or hyperactive. Electromyography is often reported as a neurogenic injury. About 5% of patients inherit defective genes through familial amyotrophic lateral sclerosis (fALS), while about 95% of patients have no known family members with the same disease, sporadic amyotrophic lateral sclerosis (sALS). Amyotrophic lateral sclerosis is currently considered to be the most challenging disease in modern medicine, and the pathogenesis of amyotrophic lateral sclerosis is lacking in definite understanding. The disease was first reported by Charles Bell (1824), but clinical and pathological descriptions were attributed to Martin Sharce (1874), who created the term "amyotrophic lateral sclerosis" for the description of muscular dystrophy-induced spinal cord sclerosis. In the united states, it is named after the very large baseball player Luge inner grid (1939) and is well known from the british famous physicist steven-hopkins (1963) that suffers from this disease. Today, people diagnosed with amyotrophic lateral sclerosis are faced with equally frustrating messages since the beol era, i.e. even with advances in molecular medicine, science and technology, there is still no effective treatment. Among neurodegenerative diseases, amyotrophic lateral sclerosis is the disease with the highest mortality rate that progresses rapidly, and dies within 2-3 years after diagnosis. After 30 years of intensive research, there is a greater understanding of its pathophysiology, but no effective treatment is available. Currently, three drugs are approved by the U.S. Food and Drug Administration (FDA), but these drugs produce serious toxic byproducts and cell damage and fail to cure the disease. At worst, this disease is heterogeneous and has no biomarkers that are validated in clinical trials, so a cut-away solution is neither viable nor measurable. Thus, there is a need to conduct multiple drug trials to address the different functional, mechanical or disability problems of the disease, which have been for many years, but unfortunately, for 200 years no one has been able to overcome the disease and survive. Current disease models are established over the past several months. To trace the origin of amyotrophic lateral sclerosis, first, the symptoms of abnormalities in the upper and lower motor neurons of the brain, spine and central nervous system are initiated. The most obvious conditions include speech and dysphagia at the onset of the medulla oblongata or limb disability, followed by lameness and progressive paralysis. Other symptoms include weight loss, cramps, respiratory failure, and tics. Changes in upper neuronal function lead to spasticity and rapid deep reflex, and symptoms of lower motor neuron abnormalities include muscle atrophy and weakness. Given that amyotrophic lateral sclerosis has no specific biomarker, diagnosis is determined by clinical features confirmed by consensus criteria. Mutation studies included the phenotype of SOD1, C9orf72 and TDP-43 Q331K in humans and mice producing pathogenic amyotrophic lateral sclerosis (Kienan 2021). Many of these mutations affect proteins involved in gene expression and regulation by transcriptional regulation, microribonucleic acid processing, ribonucleic acid (RNA) maturation and splicing. Mutations associated with amyotrophic lateral sclerosis are typically grouped according to whether they alter protein homeostasis, ribonucleic acid function, or cytoskeleton. In practice, however, high quality scientific papers and clinical trials have led to unusual "manhattan" traffic jams and frustration. Despite billions of research costs, millions of patients, tens of thousands of doctors, and best genetic and molecular research tools, the hope of curing amyotrophic lateral sclerosis is not always seen. Some examples of which are discussed in the prior art below. U.S. patent 9289459B2 discloses the use of