Abstract: The present invention provides a method for assessing the risk of drug hypersensitivity reaction caused by an antiepileptic drug with a sulfonamide derivative in a subject in need of such an assessment, comprising the step of detecting the presence of HLA-B alleles in the sample obtained from the subject, wherein the presence of the allele indicates that the subject has an increased risk of developing drug hypersensitivity reaction caused by the antiepileptic drug with the sulfonamide derivative. The present invention also provides a method for treating or reducing the incidence of such drug hypersensitivity reaction. Also provided are a test kit for assessing the risk of a patient developing drug hypersensitivity reaction caused by an antiepileptic drug with a sulfonamide derivative, comprising a reagent for determining specific HLA alleles, and use of the test kit in assessing the risk of a patient developing drug hypersensitivity reaction caused by an antiepileptic drug with a sulfonamide derivative.

Abstract: A method for assessing the risk of cutaneous adverse drug reactions (CADRs) caused by an epidermal growth factor receptor inhibitor is provided, wherein the CADRs comprises but not limited to: maculopapular eruption (MPE), erythema multiforme (EM), Stevens Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and drug rash with eosinophilia and systemic symptoms (DRESS). Also provided is a detection kit for assessing the risk of developing CADRs in patients, said kit comprising a reagent for determining specific HLA alleles and a use of the detection kit in assessing the risk of developing CADR in a patient.

Abstract: A method for assessing the risk of severe cutaneous adverse drug reactions (SCARs) induced by disease-modifying antirheumatic drugs is provided, wherein the severe cutaneous adverse drug reactions comprises but not being limited to: Stevens-Johnson Syndrome (SJS), toxic epidermal necrolysis (TEN) and drug rash with eosinophilia and systemic symptoms (DRESS). Also provided is a detection kit for assessing the risk of developing cutaneous adverse drug reactions in a subject, said kit comprising a reagent for determining specific HLA alleles and a use of the detection kit in assessing the risk of developing cutaneous adverse drug reactions in a subject.

Abstract: Provided is a method for evaluating the risk of drug hypersensitivity reaction induced by antibiotics sulfamethoxazole and/or trimethoprim. The drug hypersensitivity reaction comprises: maculopapular eruption, fixed drug eruption, Stevens-Johnson Syndrome, toxic epidermal necrolysis, drug rash with eosinophilia and systemic symptoms. A specific HLA genotype is associated with the drug hypersensitivity reaction induced by the antibiotics sulfamethoxazole and/or trimethoprim.

Abstract: A method of predicting the risk of a patient for developing phenytoin-induced adverse drug reactions (ADRs), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug reactions with eosinophilia and systemic symptoms (DRESS) is disclosed. Genetic polymorphisms of CYP2C genes (including rs1057910 (CYP2C9*3) and rs3758581 on CYP2C19), and HLA alleles (including HLA-B*1502, HLA-B*1301, and HLA-B*5101) can predict adverse reactions caused by phenytoin or fosphenytoin. Accordingly, the present invention provides a kit to assess the risk of a patient for developing adverse reactions in response to phenytoin-related drugs, which comprises the determination of the presence of a specific allele selected from the group consisting of rs1057910 (CYP2C9*3), rs3758581 on CYP2C19, HLA-B*1502, HLA-B*1301, and HLA-B*5101, wherein the presence of at least one allele is indicative of a risk for the adverse drug reactions.

Abstract: A method for assessing the risk of cutaneous adverse drug reactions induced by an anti-epileptic drug Lamotrigine is provided, wherein the cutaneous adverse drug reactions include but are not limited to: maculopapular eruption (MPE), fixed drug eruption (FDE), Stevens Johnson Syndrome (SJS), toxic epidermal necrolysis (TEN), drug rash with eosinophilia and systemic symptoms (DRESS). Further provided is a detection reagent for assessing the risk of a patient developing the cutaneous adverse drug reactions induced by the anti-epileptic drug Lamotrigine, comprising agents for measuring a particular HLA allele and the use thereof.

Abstract: Provided is a method for evaluating the risk of drug hypersensitivity reaction induced by antibiotics sulfamethoxazole and/or trimethoprim. The drug hypersensitivity reaction comprises: maculopapular eruption, fixed drug eruption, Stevens-Johnson Syndrome, toxic epidermal necrolysis, drug rash with eosinophilia and systemic symptoms. A specific HLA genotype is associated with the drug hypersensitivity reaction induced by the antibiotics sulfamethoxazole and/or trimethoprim.

Abstract: Disclosed are a method and an identification kit for identifying a causative drug for a drug hypersensitivity reaction, including: first, biological sample lymphocytes and a suspected drug or the metabolites thereof are co-cultured in vitro to form reactants, and then the expression levels of the granulysin protein, polypeptide or mRNA in the reactants are detected and compared with the control values, then the degree that the suspected drug or the metabolites thereof activate lymphocytes can be identified, thus identifying the causative drug that initiates the drug hypersensitivity reaction. The causative drug comprises Western medicine, traditional Chinese medicine, a vaccine and an antigen molecule that can cause T-cell activation.

Abstract: A method of predicting the risk of a patient for developing phenytoin-induced adverse drug reactions (ADRs), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug reactions with eosinophilia and systemic symptoms (DRESS) is disclosed. Genetic polymorphisms of CYP2C genes (including rs1057910 (CYP2C9*3) and rs3758581 on CYP2C19), and HLA alleles (including HLA-B*1502, HLA-B*1301, and HLA-B*5101) can predict adverse reactions caused by phenytoin or fosphenytoin. Accordingly, the present invention provides a kit to assess the risk of a patient for developing adverse reactions in response to phenytoin-related drugs, which comprises the determination of the presence of a specific allele selected from the group consisting of rs1057910 (CYP2C9*3), rs3758581 on CYP2C19, HLA-B*1502, HLA-B*1301, and HLA-B*5101, wherein the presence of at least one allele is indicative of a risk for the adverse drug reactions.

Abstract: The invention pertains to topical pharmaceutical formulations of berberine and its biologically equivalent analogs, such as palmatine and coptisine, for the treatment of rosacea and other red face-related skin disorders. The topical pharmaceutical formulations of this invention contain purified berberine as the primary active drug ingredient at concentrations higher than 0.1%. The invention also pertains to methods of treating rosacea and other red face related skin disorders, such as steroid-induced rosacea-like dermatitis, comprising the administration of topical pharmaceutical formulations that contain berberine or its biologically equivalent analogs, such as palmatine.

Abstract: A method of predicting the risk of a patient for developing phenytoin-induced adverse drug reactions (ADRs), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug reactions with eosinophilia and systemic symptoms (DRESS) is disclosed. Genetic polymorphisms of CYP2C genes (including rs1057910 (CYP2C9*3) and rs3758581 on CYP2C19), and HLA alleles (including HLA-B*1502, HLA-B*1301, and HLA-B*5101) can predict adverse reactions caused by phenytoin or fosphenytoin. Accordingly, the present invention provides a kit to assess the risk of a patient for developing adverse reactions in response to phenytoin-related drugs, which comprises the determination of the presence of a specific allele selected from the group consisting of rs1057910 (CYP2C9*3), rs3758581 on CYP2C19, HLA-B*1502, HLA-B*1301, and HLA-B*5101, wherein the presence of at least one allele is indicative of a risk for the adverse drug reactions.

Abstract: A method of predicting the risk of a patient for developing phenytoin-induced adverse drug reactions (ADRs), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug reactions with eosinophilia and systemic symptoms (DRESS) is disclosed. Genetic polymorphisms of CYP2C genes (including CYP2C9, CYP2C19, CYP2C8 and CYP2C18), HLA alleles (including HLA-A*0207, HLA-A*2402, HLA-B*1301, HLA-B*1502, HLA-B*4001, HLA-B*4609, HLA-B*5101, HLA-DRB1*1001 or HLA-DRB1*1502) and phenytoin concentration in the patient's plasma can all contribute to phenytoin-induced ADRs.

Abstract: A method for identifying from an HLA library an HLA complex that specifically binds to a compound. This method can be relied on to assess whether a compound is likely to induce an adverse drug reaction and, if so, in which human population.

Abstract: Disclosed are uses of granulysin in methods of diagnosing or treating autoimmune disorders.

Abstract: A method of predicting the risk of a patient for developing phenytoin-induced adverse drug reactions (ADRs), including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug reactions with eosinophilia and systemic symptoms (DRESS) is disclosed. Genetic polymorphisms of CYP2C genes (including CYP2C9, CYP2C19, CYP2C8 and CYP2C18), HLA alleles (including HLA-A*0207, HLA-A*2402, HLA-B*1301, HLA-B*1502, HLA-B*4001, HLA-B*4609, HLA-B*5101, HLA-DRB1*1001 or HLA-DRB1*1502) and phenytoin concentration in the patient's plasma can all contribute to phenytoin-induced ADRs.

Abstract: The invention pertains to topical pharmaceutical formulations of berberine and its biologically equivalent analogues, such as palmatine and coptisine, for the treatment of rosacea and other red face-related skin disorders. The topical pharmaceutical formulations of this invention contain purified berberine as the primary active drug ingredient at concentrations higher than 0.1%. The invention also pertains to methods of treating rosacea and other red face related skin disorders, such as steroid-induced rosacea-like dermatitis, comprising the administration of topical pharmaceutical formulations that contain berberine or its biologically equivalent analogues, such as palmatine.

Abstract: The present invention provides a method of predicting the risk of a patient for developing adverse drug reactions, particularly SJS or TEN. It was discovered that an HLA-B allele, HLA-B* 1502, is associated with SJS/TEN that is induced by a variety of drugs. The correlation with HLA-B* 1502 is most significant for carbamazepine-induced SJS/TEN, wherein all the patients tested have the HLA-B* 1502 allele. In addition, another HLA-B allele, HLA-B*5801, is particularly associated with SJS/TEN induced by allopurinol. Milder cutaneous reactions, such as maculopapular rash, erythema multiforme (EM), urticaria, and fixed drug eruption, are particularly associated with a third allele, HLA-B *4601. For any of the alleles, genetic markers (e.g., HLA markers, microsatellite, or single nucleotide polymorphism markers) located between DRB1 and HLA-A region of the specific HLA-B haplotype can also be used for the test.

Abstract: This invention relates to a method of determining the presence of certain HLA alleles, such as HLA-B*1502 or HLA-B*5801, and a kit for carrying out this method. Also disclosed is a method for assessing whether a patient is at risk for developing adverse drug reactions (e.g., Stevens-Johnson syndrome, toxic epidermal necrolysis, or hypersensitivity syndrome) based on the presence or absence of a genetic marker (e.g., HLA-B*1502, HLA-B*5801, or HLA-B*4601).

Abstract: A method for identifying from an HLA library an HLA complex that specifically binds to a compound. This method can be relied on to assess whether a compound is likely to induce an adverse drug reaction and, if so, in which human population.

Abstract: The present invention provides a method of predicting the risk of a patient for developing adverse drug reactions, particularly SJS or TEN. It was discovered that an HLA-B allele, HLA-B* 1502, is associated with SJS/TEN that is induced by a variety of drugs. The correlation with HLA-B* 1502 is most significant for carbamazepine-induced SJS/TEN, wherein all the patients tested have the HLA-B* 1502 allele. In addition, another HLA-B allele, HLA-B*5801, is particularly associated with SJS/TEN induced by allopurinol. Milder cutaneous reactions, such as maculopapular rash, erythema multiforme (EM), urticaria, and fixed drug eruption, are particularly associated with a third allele, HLA-B *4601. For any of the alleles, genetic markers (e.g., HLA markers, microsatellite, or single nucleotide polymorphism markers) located between DRB1 and HLA-A region of the specific HLA-B haplotype can also be used for the test.