344 Results for "

GLUT2-null hepatocytes

" in MedChemExpress (MCE) Product Catalog:
Products (344)

344 Results for "GLUT2-null hepatocytes" in MCE Product Catalog:

Cat. No.: HY-159078
CAS No.: 2607139-80-8
Purity:  98.42%
Target:  

DNA/RNA Synthesis

Research Areas:  

Cancer

PolQi1 is a selective inhibitor targeting the Polθ domain of DNA polymerase. PolQi1 inhibits the Polθ-mediated microhomology end joining (TMEJ/alt-EJ) pathway, reducing insertion/deletion (Indels) and imprecise editing events during DNA repair. PolQi1 can enhance the efficiency and accuracy of homology-directed repair (HDR) or Prime editing, and reduce off-target effects; and in combination with DNA-PK inhibitor AZD-7648 (HY-111783), exert efficient genome editing capabilities with dual pathway regulation. PolQi1 can be mainly used in gene editing research (such as CRISPR-Cas9 or Prime editing system optimization) to improve the precision editing efficiency of difficult-to-edit cells (such as primary hepatocytes and mouse embryos) [2] .
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Cat. No.: HY-183456
CAS No.: 71308-35-5
Tyrphostin AG17 is an orally active CDK2 inhibitor and EGFR tyrosine kinase antagonist. Tyrphostin AG17 reduces the levels of p21 and p16. Tyrphostin AG17 induces G1 phase cell cycle arrest, Apoptosis, mitochondrial dysfunction, decreased ATP levels, and inhibits DNA, RNA and protein synthesis, adipogenesis, and lipid synthesis. Tyrphostin AG17 inhibits fat accumulation, white adipose tissue hypertrophy, and alterations of glycogen and lipid inclusions in hepatocytes in obese mice without changing their serum biochemical parameters. Tyrphostin AG17 exhibits anticancer effects. Tyrphostin AG17 can be used in research related to immunoblastic lymphoma, leukemia, ovarian cancer, glioblastoma, colon cancer, breast cancer, melanoma, obesity and hepatic steatosis [2] .
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Cat. No.: HY-19882
CAS No.: 941285-15-0
Research Areas:  

Infection

BAL-30072 is a siderophore-bearing monocyclic β-lactam antibiotic with antibacterial activity. BAL-30072 inhibits penicillin-binding proteins 1a, 1b, and 3, thereby disrupting bacterial cell wall synthesis. BAL-30072 inhibits mitochondrial electron transport chain complex II and complex III, while also inhibiting glycolysis and mitochondrial fatty acid β-oxidation. BAL-30072 induces mitochondrial ROS production, cellular ATP depletion, reduces mitochondrial membrane potential, and triggers hepatocyte apoptosis via caspase-3/7 activation. BAL-30072 is a substrate of the hepatic uptake transporters OAT1 and OAT3. BAL-30072 can be used in research related to bacterial infections [2] .
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Cat. No.: HY-W599279
CAS No.: 2761170-84-5
ABS-752 is an orally active prodrug targeting CRBN-modulating molecular glue with selectivity in protein degradation. ABS-752 preferentially degrades GSPT1 and induces cytotoxicity through this degradation, while it also degrades NEK7, SALL4 and CK1α, with weaker degradation potency against CK1α. As a prodrug, ABS-752 requires metabolic activation to ABT-002 to form the active complex; VAP-1 mediates its conversion to an aldehyde intermediate. ABS-752 induces cell death, reduces cell viability, and exhibits antitumor activity, leading to regression and inhibition of tumor growth. ABS-752 shows no cytotoxicity in primary human hepatocytes. ABS-752 can be used in the research of hepatocellular carcinoma .
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Cat. No.: HY-W998347
CAS No.: 2922884-90-8
ABS-752 hydrochloride is an orally active prodrug targeting CRBN-modulating molecular glue with selectivity in protein degradation. ABS-752 hydrochloride preferentially degrades GSPT1 and induces cytotoxicity through this degradation, while it also degrades NEK7, SALL4 and CK1α, with weaker degradation potency against CK1α. As a prodrug, ABS-752 hydrochloride requires metabolic activation to ABT-002 to form the active complex; VAP-1 mediates its conversion to an aldehyde intermediate. ABS-752 hydrochloride induces cell death, reduces cell viability, and exhibits antitumor activity, leading to regression and inhibition of tumor growth. ABS-752 hydrochloride shows no cytotoxicity in primary human hepatocytes. ABS-752 hydrochloride can be used in the research of hepatocellular carcinoma .
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Cat. No.: HY-120657
CAS No.: 1481636-31-0
Purity:  99.88%
9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease [2] .
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Cat. No.: HY-135700
CAS No.: 19115-49-2
Purity:  ≥98.0%
Mevalonolactone is an intermediate metabolite in the eukaryotic mevalonate pathway, serving as the stable δ-lactone form of mevalonate with oral activity. Mevalonolactone exhibits binding affinity for ZNF384 (Ka = 12.6 μM) and inhibitory activity against aconitase (aconitase). Mevalonolactone promotes the nuclear localization of ZNF384 and enhances its binding to the GGPPS promoter. Mevalonolactone induces insulin resistance, disrupts glucose and lipid metabolism, enhances the isoprenylation of K-Ras, and inhibits the activation of the insulin signaling pathway. Mevalonolactone inhibits polypeptide synthesis of HMG-CoA reductase in isolated rat hepatocytes, promotes its degradation, and reduces its enzymatic activity. Mevalonolactone impairs mitochondrial function in rat brains. Mevalonolactone promotes the development of metabolically unhealthy obesity. Mevalonolactone can be used in research related to metabolically abnormal obesity, mevalonic aciduria, HMGCR-related limb-girdle myopathy, and statin-induced myopathy [2] .
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Cat. No.: HY-P2040
CAS No.: 118399-22-7
Nodularin is a hepatotoxin, tumor promoter, and protein phosphatase inhibitor. Nodularin induces apoptosis (apoptosis) in normal cells (including caspase activation, upregulation of Bcl-XS, and upregulation of BAX/P53), triggers hyperphosphorylation of the MAPK/ERK, mTOR/S6K and p38 MAPK signaling pathways, and induces oxidative stress, endoplasmic reticulum membrane instability, peroxisome proliferation and increased lysosomal enzyme activity. Nodularin promotes DEN (HY-N7434)-initiated hepatocyte proliferation and adenoma formation, and inhibits proliferation, phagocytosis and chemotaxis of normal lymphocytes, oocyte maturation and vitellogenesis, as well as angiogenesis. Nodularin exhibits hepatotoxicity, reproductive and endocrine toxicity, and embryonic developmental toxicity in various animal models. Nodularin can be used in studies related to liver cancer, hepatotoxicity and reproductive endocrine toxicity [2] .
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Cat. No.: HY-W019704R
CAS No.: 1115-47-5
N-Acetyl-DL-methionine (Standard) is the analytical standard of N-Acetyl-DL-methionine (HY-W019704). This product is intended for research and analytical applications. N-Acetyl-DL-methionine is an orally active methionine analog and a glutathione (GSH) precursor that can be metabolized into cysteine in vivo. N-Acetyl-DL-methionine increases plasma methionine concentration and the molar percentage of plasma lysine in castrated sheep, and can partially meet the methionine requirement of growing rats. N-Acetyl-DL-methionine is absorbable from the lower digestive tract of sheep and undergoes ruminal microbial degradation in vivo. N-Acetyl-DL-methionine alleviates Acetaminophen (HY-66005)-induced hepatic GSH depletion in mice, maintains hepatocyte integrity, and promotes de novo synthesis of hepatic GSH. N-Acetyl-DL-methionine can be used in studies related to acetaminophen-induced liver injury [2].
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Cat. No.: HY-113308AS1
CAS No.: 1265476-97-8
Taurolithocholic Acid-d5 (sodium) is the deuterium labeled Taurolithocholic acid sodium salt. Taurolithocholic Acid sodium salt is an orally active bile acid and antiviral agent. Taurolithocholic Acid sodium salt upregulates FADS2 by activating the TGR5-PI3K/AKT-SREBP2 signaling axis, inhibits SFTSV-induced ferroptosis, viral replication and viral entry of HBV/HDV, while reducing the release of IL-1β, lipid ROS and LDH. While exerting antiviral protective effects, Taurolithocholic Acid sodium salt also stimulates the recycling of hepatocellular membrane transporters, impairs canalicular bile acid secretion function, and induces hepatocyte cholestasis, apoptosis and acute hepatocellular injury. Taurolithocholic Acid sodium salt serves as an experimental model compound for hepatocellular cholestasis. At concentrations ≤200 μM, Taurolithocholic Acid sodium salt shows no cytotoxicity and does not activate the interferon pathway. Taurolithocholic Acid sodium salt not only protects mice from lethal SFTSV infection but also is suitable for studies related to severe fever with thrombocytopenia syndrome and cholestasis [2] .
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Cat. No.: HY-113308AS2
Taurolithocholic acid-d4-1 (sodium) is the deuterium labeled Taurolithocholic acid. Taurolithocholic acid sodium is an orally active bile acid and antiviral agent. Taurolithocholic acid sodium upregulates FADS2 by activating the TGR5-PI3K/AKT-SREBP2 signaling axis, inhibits SFTSV-induced ferroptosis, viral replication and viral entry of HBV/HDV, while reducing the release of IL-1β, lipid ROS and LDH. While exerting antiviral protective effects, Taurolithocholic acid sodium also stimulates the recycling of hepatocellular membrane transporters, impairs canalicular bile acid secretion function, and induces hepatocyte cholestasis, apoptosis and acute hepatocellular injury. Taurolithocholic acid sodium serves as an experimental model compound for hepatocellular cholestasis. At concentrations ≤200 μM, Taurolithocholic acid sodium shows no cytotoxicity and does not activate the interferon pathway. Taurolithocholic acid sodium not only protects mice from lethal SFTSV infection but also is suitable for studies related to severe fever with thrombocytopenia syndrome and cholestasis [2] .
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Cat. No.: HY-113308S
CAS No.: 1265681-64-8
Taurolithocholic acid-d5 is deuterium labeled Taurolithocholic acid. Taurolithocholic acid is an orally active bile acid and antiviral agent. Taurolithocholic acid upregulates FADS2 by activating the TGR5-PI3K/AKT-SREBP2 signaling axis, inhibits SFTSV-induced ferroptosis, viral replication and viral entry of HBV/HDV, while reducing the release of IL-1β, lipid ROS and LDH. While exerting antiviral protective effects, Taurolithocholic acid also stimulates the recycling of hepatocellular membrane transporters, impairs canalicular bile acid secretion function, and induces hepatocyte cholestasis, apoptosis and acute hepatocellular injury. Taurolithocholic acid serves as an experimental model compound for hepatocellular cholestasis. At concentrations ≤200 μM, Taurolithocholic acid shows no cytotoxicity and does not activate the interferon pathway. Taurolithocholic acid not only protects mice from lethal SFTSV infection but also is suitable for studies related to severe fever with thrombocytopenia syndrome and cholestasis [2] .
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Cat. No.: HY-154974
CAS No.: 2408140-60-1
Purity:  ≥95.0%
Target:  

Liposome

Research Areas:  

Cancer

LNP Lipid-8 (11-A-M) is an ionizable single-tail multi-head lipid that can be used as a lipid nanoparticle (LNP) to deliver siRNA to T cells without targeting ligands. LNP Lipid-8 is more selective for T cells than other cell types such as hepatocytes. LNP Lipid-8 selectively delivers siRNA/sgRNA to T cells (especially CD8+ T cells) through endogenous lipid transport pathways, and can enter cells and release RNA through endocytosis to achieve gene silencing. LNP Lipid-8 loaded with GFP siRNA (siGFP) significantly led to GFP gene silencing in mouse models. LNP Lipid-8 showed good efficacy and safety in both cells and animals, without obvious liver targeting and toxicity. LNP Lipid-8 can be used for RNA delivery research in the fields of tumor immunotherapy and T cell-mediated autoimmune diseases .
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Cat. No.: HY-178371
Target:  

PI3K

Research Areas:  

Metabolic Disease

PI3KC2γ-IN-1 (Compound 23) is an orally active and selective PI3KC2γ inhibitor (IC50 = 4 nM). PI3KC2γ-IN-1 downregulats the Akt2-glycogen synthase (GS) signaling pathway, ultimately inhibiting the conversion of glucose to glycogen and reduces excessive glycogen accumulation in the liver. PI3KC2γ-IN-1 can significantly inhibit insulin-induced PI(3,4)P2 accumulation in both primary hepatocytes and HepG2 liver cancer cells. PI3KC2γ-IN-1 can be used for the study of glycogen storage diseases (GSDs) .
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Cat. No.: HY-P992072

Target:  

Apoptosis Caspase

Research Areas:  

Metabolic Disease

Anti-Human/Mouse CD95 Antibody (HFE7A) is an antibody targeting human/mouse Fas (CD95), with a Kd of 1.6 nM in mice. Anti-Human/Mouse CD95 Antibody (HFE7A) modulates the Fas-mediated apoptotic signaling pathway without blocking the binding of Jo2 to Fas. Anti-Human/Mouse CD95 Antibody (HFE7A) inhibits Jo2-induced caspase activation, mitochondrial depolarization, hepatocyte death and apoptosis. Anti-Human/Mouse CD95 Antibody (HFE7A) protects BALB/c mice against Jo2-induced acute liver injury and reduces Jo2-associated elevation of serum transaminase levels. Anti-Human/Mouse CD95 Antibody (HFE7A) can be used in studies related to liver injury. For isotype control, refer to Mouse IgG1 kappa, Isotype Control (HY-P99977) .
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Cat. No.: HY-W770410
CAS No.: 2748638-71-1
9-PAHSA- 13C4 is 13C-labeled 9-PAHSA. 9-PAHSAis an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSAsignificantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSAinduces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSAregulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSAdoes not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSAcan be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease [2] .
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Cat. No.: HY-113308AR
CAS No.: 6042-32-6
Taurolithocholic acid (sodium salt) (Standard) is the analytical standard of Taurolithocholic acid (sodium salt). This product is intended for research and analytical applications. Taurolithocholic acid sodium salt is an orally active bile acid and antiviral agent. Taurolithocholic acid sodium salt upregulates FADS2 by activating the TGR5-PI3K/AKT-SREBP2 signaling axis, inhibits SFTSV-induced ferroptosis, viral replication and viral entry of HBV/HDV, while reducing the release of IL-1β, lipid ROS and LDH. While exerting antiviral protective effects, Taurolithocholic acid sodium salt also stimulates the recycling of hepatocellular membrane transporters, impairs canalicular bile acid secretion function, and induces hepatocyte cholestasis, apoptosis and acute hepatocellular injury. Taurolithocholic acid sodium salt serves as an experimental model compound for hepatocellular cholestasis. At concentrations ≤200 μM, Taurolithocholic acid sodium salt shows no cytotoxicity and does not activate the interferon pathway. Taurolithocholic acid sodium salt not only protects mice from lethal SFTSV infection but also is suitable for studies related to severe fever with thrombocytopenia syndrome and cholestasis [2] .
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Cat. No.: HY-120657R
CAS No.: 1481636-31-0
Flumethrin (Standard) is the analytical standard of Flumethrin. This product is intended for research and analytical applications. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease [2] .
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Cat. No.: HY-120657S
CAS No.: 2704278-85-1
9-PAHSA-d4 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease [2] .
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Cat. No.: HY-120657S1
CAS No.: 2748208-06-0
9-PAHSA-d31 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease [2] .
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