β-catenin Activator

Notoginsenoside R2 (20(S)-Notoginsenoside R2; Ginsenoside Ng-R2) is an orally active notoginsenoside. Notoginsenoside R2 activates P90RSK and Nrf2 via the MEK1/2-ERK1/2 pathway to inhibit 6-OHDA-induced apoptotic damage in nerve cells. Notoginsenoside R2 upregulates SOX8/β-catenin by reducing miR-27a, thereby suppressing Aβ_25-35-induced neuronal apoptosis and inflammatory responses. Notoginsenoside R2 alleviates lipid accumulation and mitochondrial dysfunction in diabetic nephropathy by inhibiting c-Src. Notoginsenoside R2 alleviates hepatic fibrosis by inducing hepatic stellate cell senescence and inhibiting the inflammatory microenvironment via JAK/STAT3 suppression. Notoginsenoside R2 can be used in research related to Parkinson's disease, Alzheimer's disease, diabetic nephropathy and hepatic fibrosis.

Withanolide B is an active component of W. somnifera Dunal. Withanolide B promotes osteogenic differentiation of hBMSCs via ERK1/2 and Wnt/β-catenin signaling pathways. Withanolide B exhibits neuroprotective, anti-arthritic, anti-aging and anti-cancer effects.

Ciprofloxacin (Standard) is the analytical standard of Ciprofloxacin. This product is intended for research and analytical applications. Ciprofloxacin (Bay-09867) is an orally active, blood-brain barrier permeable fluoroquinolone antibacterial agent. Ciprofloxacin exerts bactericidal effects primarily by inhibiting topoisomerase II and IV. Ciprofloxacin inhibits the proliferation of human dental pulp stem cells and chondrocytes from young rats, and also activates the Akt signaling pathway and upregulates markers such as β-catenin and Nanog to maintain the morphological characteristics of stem cells. Ciprofloxacin induces significant neurotoxicity and tissue damage, including reducing serotonin and glutathione levels in the brain, inducing oxidative stress and depression-like behaviors, and causing articular cartilage damage. Ciprofloxacin can be applied to research related to infections of necrotic young permanent teeth and neurotoxicity.

Perfluoroundecanoic acid is a perfluoroalkyl substance (PFAS). Perfluoroundecanoic acid is an orally active oxidative stress inducer. Perfluoroundecanoic acid promotes macrophage M2 polarization, activates Wnt/β-catenin signaling and enhances β-catenin nuclear accumulation. Perfluoroundecanoic acid -induced M2 phenotype macrophage accelerates tumor progression in vitro and in vivo. Perfluoroundecanoic acid induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice. Perfluoroundecanoic acid inhibits Leydig cell development in pubertal male rats via inducing oxidative stress and autophagy. Perfluoroundecanoic acid accelerates insulitis development in a mouse model of type 1 diabetes. Perfluoroundecanoic acid can be used for the study of ovarian cancer, type 1 diabetes and inflammation.

Mirodenafil (SK3530) is an orally active, potent, reversible, and selective phosphodiesterase 5 (PDE5) inhibitor. Mirodenafil is a glucocorticoid receptor (GR) modulator Mirodenafil activates the Wnt/β-catenin signaling pathway by downregulating Dkk1 expression. Mirodenafil can be used for the research of erectile dysfunction (ED), Alzheimer’s disease (AD) and systemic sclerosis (SSc).

Viridicatol is a quinolone alkaloid with anti-inflammatory, antibacterial, antifungal, osteogenic and chondrogenic activities. Viridicatol reduces the phosphorylation levels of ERK, JNK, p38 and STAT6; inhibits MMP-2, MMP-9, NF-κB signaling pathway and PTP1B; downregulates genes related to mast cell activation; and binds to SHN3 to activate the Wnt/SHN3 signaling pathway. Viridicatol inhibits the expression of pro-inflammatory mediators and cytokines, and promotes osteogenic/chondrogenic differentiation. Viridicatol can be used in studies related to fibrosarcoma, allergy, bacterial infection, fungal infection and osteoporosis.

Nocardamine (Desferrioxamine E; Nocardamin) is a cyclic trihydroxamate siderophore with iron ion chelation, antioxidant, antibacterial and other activities. Nocardamine is synthesized by Pseudomonas stutzeri under iron-deficient conditions, and excessive iron ions significantly inhibit its biosynthesis process. Nocardamine increases the level of phosphorylated ERK protein, promotes nuclear translocation of β-catenin, and restores the downregulated expression of SIRT1 protein. Nocardamine alleviates cellular oxidative stress, reduces ROS content, and simultaneously repairs the ability to form mineralized nodules and the expression of osteogenic markers. Nocardamine induces FoxA gene transcription and protein expression to assist Pseudomonas aeruginosa in iron ion uptake; it also selectively inhibits the proliferation of mycobacteria. Nocardamine induces spindle-shaped morphological changes in BM-N4 insect cells, and sufficient iron ions inhibit this cellular morphological change. Nocardamine is suitable for research related to bacterial infections.

Chrysosplenetin is an orally active polymethoxyflavone. Chrysosplenetin exerts anticancer effects by inhibiting topoisomerase, protecting DNA and inducing apoptosis. Chrysosplenetin acts as an antimalarial sensitizer, reverses Artemisinin (HY-B0094) resistance by inhibiting and downregulating P-glycoprotein, and enhances the efficacy of Artemisinin. Chrysosplenetin promotes bone formation by activating the Wnt/β-catenin pathway and exerts anti-osteoporotic effects.

(E)-Ferulic acid-d₃ is the deuterium labeled (E)-Ferulic acid. (E)-Ferulic acid is a isomer of Ferulic acid which is an aromatic compound, abundant in plant cell walls. (E)-Ferulic acid causes the phosphorylation of β-catenin, resulting in proteasomal degradation of β-catenin and increases the expression of pro-apoptotic factor Bax and decreases the expression of pro-survival factor survivin. (E)-Ferulic acid shows a potent ability to remove reactive oxygen species (ROS) and inhibits lipid peroxidation. (E)-Ferulic acid exerts both anti-proliferation and anti-migration effects in the human lung cancer cell line H1299.

Soyasaponin Ba is a soyasaponin that can be isolated from Phaseolus vulgaris, acts as an aldose reductase inhibitor (ARI). Soyasaponin Ba activates Akt/GSK3β/β-catenin signaling pathway, reduces lipid accumulation, lowers ROS generation, improves mitochondrial membrane potential, ATP levels, and morphology, and inhibits apoptosis. Soyasaponin Ba can be used for the research of lipid accumulation and secondary diabetic complications.

GSK3β-IN-2 (Compound S01) is the inhibitor for GSK3β with an IC₅₀ of 0.35 nM. GSK3β-IN-2 activates Wnt/β-catenin signaling pathway, promotes neurogenesis and neurite growth. GSK3β-IN-2 inhibits Aβ-induced tau hyperphosphorylation at Ser396, reduces the formation of neurofibrillary tangles. GSK3β-IN-2 ameliorates Alzheimer's Disease in zebrafish model.

WAY-362692 is a secreted frizzled-related protein (sFRP-1) inhibitor (IC₅₀ of 0.02 μM), targeting the netrin domain of sFRP-1. WAY-362692 can competitively inhibit the interaction between sFRP-1 and Wnt proteins, and activate the Wnt/β-catenin signaling pathway (EC₅₀ = 0.03 μM). WAY-362692 can activate osteoblasts and promote bone remodeling. WAY-362692 can be used for the research of metabolic disease, such as osteoporosis.

Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC₅₀ values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases.

Nodakenetin is an orally active Wnt/β-catenin pathway activator. Nodakenetin reduces the level of DKK1, and upregulates c-Myc, cyclin D1 and survivin. Nodakenetin induces osteoprogenitor cell differentiation, upregulates bone formation biomarkers and prevents bone microstructure degeneration. Nodakenetin induces irritant skin reactions. Nodakenetin improves bone microstructure and histomorphometric parameters in osteoporotic mouse models. Nodakenetin can be used for osteoporosis-related research.

Hordenine hydrochloride (Ordenina hydrochloride; Peyocactine hydrochloride) is a multifunctional alkaloid with oral activity and blood-brain barrier penetration. Hordenine hydrochloride inhibits LPS-induced phosphorylation of p38, JNK, ERK1/2, p65, IκB, and AKT, prevents p65 nuclear translocation, and suppresses inflammatory cytokines and mediators. Hordenine hydrochloride promotes M2 macrophage polarization, restores blood-milk barrier integrity, alleviates oxidative stress by reducing ROS and MDA, and attenuates LPS-induced lung injury and pulmonary edema. Hordenine hydrochloride inhibits cAMP production, CREB phosphorylation, and MITF expression, thereby suppressing melanin synthesis in melanocytes and reconstructed epidermis. Hordenine hydrochloride activates the Wnt/β-catenin signaling pathway, promotes dermal papilla cell proliferation and hair shaft elongation, and accelerates hair regeneration. Hordenine hydrochloride activates DRD2, acts as a D3R partial agonist, α2A-AR full agonist, and 5-HT2A-R antagonist, and inhibits SERT and DAT. Hordenine hydrochloride inhibits α-synuclein accumulation and ameliorates motor deficits in Parkinson's disease models. Hordenine hydrochloride limits alcohol intake, reduces relapse drinking behavior, and modulates alcohol-induced conditioned place preference. Hordenine hydrochloride can be used for research on mastitis, skin pigmentation, acute lung injury, foodborne diseases, hair loss, Parkinson's disease, bacterial infections, and alcohol use disorder.

Hordenine-d₆ (Ordenina-d₆; Peyocactine-d₆) is the deuterated-labeled Hordenine (HY-N0113). Hordenine (Ordenina; Peyocactine) is a multifunctional alkaloid with oral activity and blood-brain barrier penetration. Hordenine inhibits LPS-induced phosphorylation of p38, JNK, ERK1/2, p65, IκB, and AKT, prevents p65 nuclear translocation, and suppresses inflammatory cytokines and mediators. Hordenine promotes M2 macrophage polarization, restores blood-milk barrier integrity, alleviates oxidative stress by reducing ROS and MDA, and attenuates LPS-induced lung injury and pulmonary edema. Hordenine inhibits cAMP production, CREB phosphorylation, and MITF expression, thereby suppressing melanin synthesis in melanocytes and reconstructed epidermis. Hordenine activates the Wnt/β-catenin signaling pathway, promotes dermal papilla cell proliferation and hair shaft elongation, and accelerates hair regeneration. Hordenine activates DRD2, acts as a D3R partial agonist, α2A-AR full agonist, and 5-HT2A-R antagonist, and inhibits SERT and DAT. Hordenine inhibits α-synuclein accumulation and ameliorates motor deficits in Parkinson's disease models. Hordenine limits alcohol intake, reduces relapse drinking behavior, and modulates alcohol-induced conditioned place preference. Hordenine can be used for research on mastitis, skin pigmentation, acute lung injury, foodborne diseases, hair loss, Parkinson's disease, bacterial infections, and alcohol use disorder.

PTD-DBM is a CXXC5-Dvl protein-protein interaction inhibitor and also a Wnt/β-catenin pathway activator. PTD-DBM interferes with the Dvl-binding function of CXXC5, disrupts the negative feedback regulation of the Wnt/β-catenin pathway, induces β-catenin expression and nuclear translocation, and increases the production of type I collagen, α-smooth muscle actin and endothelin-1. PTD-DBM is applicable to studies related to androgenetic alopecia and skin wound healing.

Cardiogenol C hydrochloride is a potent cell-permeable pyrimidine inducer which prompts the differentiation of ESCs into cardiomyocytes (EC₅₀=100 nM). Cardiogenol C hydrochloride also acts cardiomyogenic on already lineage-committed progenitor cell types with a limited degree of plasticity. Cardiogenol C hydrochloride is a useful cardiomyogenic agent and can be used as a tool to improve cardiac repair by cell transplantation therapy in animal models.

Evabosmig (AGA2118) is a humanized bispecific monoclonal antibody targeting sclerostin (SOST/sclerostin) and DKK1. SOST and DKK1 are two key secreted negative regulators of the intramedullary Wnt/β-catenin pathway. Evabosmig possesses activities to induce bone formation, inhibit bone resorption and increase bone mineral density. Evabosmig is applicable for research related to osteoporosis.

RMC-9945 (RM-044) is a selective, covalent, and orally active RAS (ON) G12D inhibitor. RMC-9945 enhances the transcriptional activity of β-Catenin/TCF. RMC-9945 induces cell state transition, forcing metastatic colorectal cancer cells to switch from the Emp1⁺ state to the Lgr5⁺ stem cell-like state. RMC-9945 achieves durable disease control in preclinical models of colorectal cancer with early liver metastasis, but shows reduced activity in late-stage metastasis models. RMC-9945 can be used in research related to metastatic colorectal cancer and pancreatic ductal adenocarcinoma.