Allergy

Diphenhydramine hydrochloride is a first-generation histamine H1-receptor antagonist with anti-cholinergic effect. Diphenhydramine hydrochloride can across the ovine blood-brain barrier (BBB).

Difelikefalin (CR-845; FE-202845) is an orally active peripherally acting kappa opioid receptor agonist. Difelikefalin reduces acute kidney injury, decreases oliguria, maintains urine flow, inhibits cytokine expression, and improves survival in endotoxemia after ischemia/reperfusion. Difelikefalin suppresses pruritus signals and exhibits neuromodulatory antipruritic activity. Difelikefalin can be used in research related to acute kidney injury, chronic kidney disease-associated pruritus, and atopic dermatitis.

Mepyramine maleate (Pyrilamine maleate) is a selective histamine H1 receptor antagonist and KCNQ channel inhibitor, with an IC₅₀ of 12.5 μM against KCNQ2/Q3. Mepyramine maleate shows no activity against allergic asthma in mice when used alone, but modulates the effect of JNJ 7777120 (HY-13508) on allergic asthma in mice; it inhibits the development of morphine physical dependence and increases histamine levels in mouse brains. Mepyramine maleate can be used in studies related to seizures, convulsions, allergic asthma and morphine physical dependence.

Ketotifen (HC 20-511) is an orally active second-generation noncompetitive histamine 1 (H1) receptor blocker and mast cell stabilizer. Ketotifen can block 6-phosphogluconate dehydrogenase (PGD) in vitro. Ketotifen also has antiviral activity against SARS-CoV-2 and Influenza virus. Ketotifen can be used to the research of autoimmune encephalomyelitis (EAE) and asthma attack prevention.

Bempikibart (ADX-914) is a fully human IgG1-κ monoclonal antibody targeting IL-7Rα. Bempikibart binds to the IL-7 receptor alpha and blocks IL-7 and TSLP signaling. Bempikibart reduces T cell populations while relatively preserving regulatory T cells. Bempikibart inhibits Th1, Th2, and Th17 immune pathways. Bempikibart can be used in research on alopecia areata and atopic dermatitis.

Ligelizumab (QGE 031) is a humanized high-affinity anti-immunoglobulin IgE monoclonal antibody. Ligelizumab selectively inhibits the binding of IgE to the high-affinity receptor FcεRI, while the inhibitory effect on the low-affinity receptor CD23 is weak. Ligelizumab can inhibit the activation of effector cells such as mast cells and Basophil, while reducing the production of IgE by B cells, and restoring the IFN-α production and regulatory T cell (Treg) induction function of plasmacytoid dendritic cells (pDC). Ligelizumab can be used in the study of allergic diseases (such as chronic spontaneous urticaria, allergic asthma).

Dodecanoylcarnitine ((-)-Lauroylcarnitine) is a medium long-chain acylcarnitine, an intermediate product in key energy metabolic pathways of fatty acid β-oxidation and amino acids catabolism. The abnormal decrease in the Dodecanoylcarnitine levels indicats that mitochondrial fuel metabolism, including fatty acid oxidation is significantly disturbed. Changes in plasma concentrations of Dodecanoylcarnitine are not only associated with type II diabetes, but also with pre-diabetes status. Dodecanoylcarnitine is present in fatty acid oxidation disorders such as long-chain acyl CoA dehydrogenase deficiency, carnitine palmitoyltransferase I/II deficiency, and is also associated with celiac disease. Dodecanoylcarnitine deomonstrates high sensitivities and specificities in predicting asthma. Combined model of Decanoylcarnitine (HY-113069), Dodecanoylcarnitine, PC (16:0/0:0), and Asp Arg Pro can be used as a potential biomarker for the diagnosis of Yin-deficiency-heat syndrome.

Temtokibart (ARGX-112) is a monoclonal antibody and also an IL-22RA1 inhibitor. Temtokibart inhibits the signal transduction of IL-22, IL-20 and IL-24. Temtokibart reduces the expression levels of inflammatory proteins, chemokines, immune cell migration and markers of activated immune pathways. Temtokibart improves the expression of genes related to immunity and epidermal barrier function. Temtokibart is applicable to research on moderate-to-severe atopic dermatitis.

Doxepin Hydrochloride is an orally active, blood-brain barrier penetrant tricyclic antidepressant with multiple activities including hypnosis, sedation, analgesia and vasodilation. Doxepin Hydrochloride enhances the expression of PSD-95 and synapsin 1 via the PI3K/AKT/mTOR signaling pathway, and is metabolized to DesmethylDoxepin Hydrochloride in vivo. Doxepin Hydrochloride can be used in research related to various diseases such as depression, anxiety, obesity and atopic dermatitis.

Quilizumab (Anti-Human IGHE Recombinant Antibody; 47H4; MEMP1972A) is a monoclonal antibody that targets FcγRIIIa and the M1 prime segment of human membrane-bound IgE. Quilizumab has enhanced FcγRIIIa binding affinity and activity against IgE class-switched B cells, and reduces serum IgE levels by inducing antibody-dependent cell-mediated cytotoxicity and apoptosis through cross-linking of membrane-bound IgE receptors. Quilizumab depletes IgE-producing cells; it also directly binds the membrane-bound M1 prime domain on IgE class-switched cells to inhibit IgE production. Quilizumab is used in research on allergic asthma and allergic diseases (asthma, allergic rhinitis).

Lokivetmab (Anti-Canine IL31 Recombinant Antibody) is an anti-canine IL-31 monoclonal antibody. Lokivetmab inhibits IL-31-mediated activation of pruritogenic signals in peripheral sensory neurons and reduces TH2-weighted inflammation. Lokivetmab demonstrates long-term efficacy in controlling pruritus and improving skin lesions in dogs with canine atopic dermatitis (CAD). Lokivetmab can be used for the research of atopic dermatitis (AD) in dogs.

Anti-Mouse TSLP Antibody (28F12) is an anti-mouse TSLP IgG2a monoclonal antibody. Anti-Mouse TSLP Antibody (28F12) weakens skin inflammation and allergic reactions by reducing Treg cells and lymph node cells. Anti-Mouse TSLP Antibody (28F12) can be used for research on allergic conditions.

Isobavachin is an orally active, blood-brain barrier-penetrating prenylated flavonoid present in Psoralea corylifolia. Isobavachin inhibits human CYP2B6, CYP2C9, CYP2C19, UGT1A1, UGT1A9, and UGT2B7. Isobavachin suppresses MAPK activation, NF-κB nuclear translocation, overexpression of iNOS/COX-2, FcεRI-mediated signaling pathways, and RANKL-induced osteoclastogenesis. Isobavachin induces autophagy, cytotoxicity, neuronal differentiation, and NRF2 activation; it alleviates oxidative damage, inflammatory responses, apoptosis, iron accumulation, mitochondrial biogenesis, and mast cell degranulation. Isobavachin is applicable to research related to liver injury, inflammatory diseases, osteoporosis, liver cancer, prostate cancer, glioma, periodontitis-induced bone loss, and Alzheimer's disease.

Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota. Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma.

Ganoderma Lucidum/Reishi Extract is a Ganoderma lucidum extract. Ganoderma Lucidum/Reishi Extract reduces the expression of c-Myc, BCL-2, BCL-XL, TERT, PDGFB, eIF4G, Survivin, β-catenin, and eIF4E. Ganoderma Lucidum/Reishi Extract downregulates the gene expression of MMP-9. Ganoderma Lucidum/Reishi Extract upregulates the expression of IL8. Ganoderma Lucidum/Reishi Extract is applicable to the research of inflammatory breast cancer. Ganoderma Lucidum is used in the research of various diseases, such as allergy, arthritis, hypertension, neurasthenia, inflammation, and cancer.

CMIT/MIT (14.5% in water) (CMI/MI) is a mixture of CMIT and MIT, and is also a preservative and skin sensitizer. CMIT/MIT (14.5% in water) increases the levels of phosphorylated ERK1/2, p38, JNK1/2, p53, p21 and Bax, decreases the level of Bcl-2, and activates the Nrf-2/HO-1 signaling pathway. CMIT/MIT (14.5% in water) increases LDH release and lipid peroxidation levels, impairs antioxidant defense capacity, promotes pro-inflammatory cytokine release, induces apoptosis, triggers cell cycle arrest, exhibits neurotoxicity in neuroblastoma cells, and causes dysregulation of Th2/Th17 immune responses. CMIT/MIT (14.5% in water) can be used in studies related to allergy, atopic dermatitis and lung injury.

Atinvicitinib is an orally active and selective JAK1 inhibitor. Atinvicitinib blocks signaling of JAK1-dependent pruritogenic and pro-inflammatory cytokines, including those in the IL-31, IL-4, and IL-13 pathways. Atinvicitinib can be used for the researches of pruritus associated with allergic dermatitis and canine atopic dermatitis.

PROTAC HSP90 degrader BP3 is a potent and selective degradation of HSP90 in a CRBN-dependent fashion. PROTAC HSP90 degrader BP3 has a certain degradation effect on HSP90 protein in MCF-7 cells (DC₅₀=0.99 μM). PROTAC HSP90 degrader BP3 inhibits the growth of breast cancer cell. PROTAC HSP90 degrader BP3 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

Melrilimab (GSK 3772847; CNTO-7160) is a humanized IgG2σ monoclonal antibody that targets the IL-33 receptor ST2 and blocks the IL-33/ST2 signaling pathway by binding to the ST2 protein. Melrilimab is applicable to research related to asthma and atopic dermatitis.

Sphingosylphosphorylcholine is a bioactive lipid and a major component of plasma high-density lipoprotein that binds to OGR1 with a K_d of 33.3 nM. Sphingosylphosphorylcholine triggers delayed phosphorylation of Smad2, upregulates α-SMA expression, and activates TRPM3. Sphingosylphosphorylcholine reduces Apoptosis and upregulates the expression of uPA and its receptor uPA-R. Sphingosylphosphorylcholine exerts anti-apoptotic, anti-cardiac hypertrophy and pro-wound healing effects. Sphingosylphosphorylcholine induces scratching behavior in mice. Sphingosylphosphorylcholine is used in studies related to atopic dermatitis, promyelocytic leukemia, heart failure, myocardial ischemia/reperfusion injury, ovarian cancer, breast cancer, pancreatic cancer, and skin wound healing disorders in genetically impaired healing diabetes.