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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
2186 Results for "
Cell level
" in MedChemExpress (MCE) Product Catalog:
Products (2186)
2186 Results for "Cell level" in MCE Product Catalog:
902
Research Areas:
Z-VAD-FMK is a pan-caspase inhibitor and also an ICE-like protease inhibitor, which inhibits apoptosis by preventing the processing of CPP32 to its active form. Z-VAD-FMK sensitivity varies primarily due to differential expression of receptor-interacting protein 1 (RIP1). Z-VAD-FMK limits the cryopreservation-induced apoptosis by reducing caspase-3 activity of in vitro produced bovine embryos. Z-VAD-FMK is immunosuppressive in vitro and inhibits T cell proliferation without blocking the processing of caspase-8 and caspase-3. Z-VAD-FMK leads to a decrease in intracellular glutathione (GSH) with a concomitant increase in reactive oxygen species (ROS) levels in activated T cells. Z-VAD-FMK is due to oxidative stress via the depletion of GSH. Z-VAD-FMK can be used for the study of acute pancreatitis .
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525 Cited Publications
Target:
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MK-2206 is an orally active pan-AKT inhibitor, with IC50 values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .
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525 Cited Publications
Synonyms: MK-2206 (2HCl)
Target:
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MK-2206 dihydrochloride (MK-2206 2HCl) is an orally active pan-AKT inhibitor, with IC50 values of 8 nM, 12 nM and 65 nM against AKT1, AKT2 and AKT3, respectively. MK-2206 dihydrochloride inhibits the Akt/mTOR signaling pathway and reduces the levels of downstream GSK3β and Mcl-1 via proteasomal degradation. MK-2206 dihydrochloride induces G1-phase cell cycle arrest, apoptosis, epithelial-mesenchymal transition, fibroblast activation and extracellular matrix deposition. MK-2206 dihydrochloride causes transient hyperglycemia and hyperinsulinemia in animals. MK-2206 dihydrochloride can be used in research related to solid tumors, renal fibrosis and hypercholesterolemia .
476
476 Cited Publications
Synonyms: Desferrioxamine B mesylate; DFOM
Research Areas:
Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Deferoxamine mesylate (Deferoxamine B mesylate) is an iron chelator (binds to Fe(III) and many other metal cations), is widely used to reduce iron accumulation and deposition in tissues. Deferoxamine mesylate upregulates HIF-1α levels with good antioxidant activity. Deferoxamine mesylate also shows anti-proliferative activity, can induce apoptosis and autophagy in cancer cells. Deferoxamine mesylate can be used in studies of diabetes, neurodegenerative diseases as well as anti-cancer and anti-COVID-19 .
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476 Cited Publications
Synonyms: Deferoxamine B; Deferriferrioxamine B; Deferrioxamine
Research Areas:
Deferoxamine (Deferoxamine B) is an iron chelator (binds to Fe(III) and many other metal cations), is widely used to reduce iron accumulation and deposition in tissues. Deferoxamine upregulates HIF-1α levels with good antioxidant activity. Deferoxamine also shows anti-proliferative activity, can induce apoptosis and autophagy in cancer cells. Deferoxamine can be used in studies of diabetes, neurodegenerative diseases as well as anti-cancer and anti-COVID-19 .
328
Target:
Raf VEGFR FLT3 Autophagy Apoptosis STAT Akt MMP Cadherin p38 MAPK ERK MEK PI3K PARP Bcl-2 Family Ephrin Receptor PDGFR c-Kit
Research Areas:
Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma .
328
328 Cited Publications
Synonyms: Bay 43-9006 tosylate
Target:
Raf VEGFR FLT3 Autophagy Apoptosis STAT Akt MMP Cadherin p38 MAPK ERK MEK PI3K PARP Bcl-2 Family Ephrin Receptor PDGFR c-Kit
Research Areas:
Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Sorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma .
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Temozolomide (NSC 362856) is an oral active DNA alkylating agent that crosses the blood-brain barrier. Temozolomide is also a proautophagic and proapoptotic agent. Temozolomide is effective against tumor cells that are characterized by low levels of O6-alkylguanine DNA alkyltransferase (OGAT) and a functional mismatch repair system. Temozolomide has antitumor and antiangiogenic effects .
176
176 Cited Publications
Synonyms: Tetraethylthiuram disulfide; TETD
Research Areas:
Disulfiram (Tetraethylthiuram disulfide) is a specific inhibitor of aldehyde-dehydrogenase (ALDH1), used for the treatment of chronic alcoholism by producing an acute sensitivity to alcohol. Disulfiram inhibits gasdermin D (GSDMD) pore formation in liposomes and inflammasome-mediated pyroptosis and IL-1β secretion in human and mouse cells. Disulfiram, a copper ion carrier, with Cu 2+ increases intracellular ROS levels and induces cuproptosis .
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Target:
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Pirfenidone (AMR69) is an antifibrotic agent that attenuates CCL2 and CCL12 production in fibrocyte cells. Pirfenidone has growth-inhibitory effect and reduces TGF-β2 protein levels in human glioma cell lines. Pirfenidone also has anti-inflammatory activities .
78
Target:
Research Areas:
Cilengitide (EMD 121974) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC50 values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors .
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Target:
Research Areas:
Cilengitide TFA (EMD 121974 TFA) is an integrin (integrin) inhibitor with blood-brain barrier permeability, with IC50 values against human targets as follows: 0.61 nM for αvβ3, 8.4 nM for αvβ5, 14.9 nM for α5β1, 5400 nM for αIIbβ3, 2050 nM for αvβ6, 2350 nM for αvβ8. Cilengitide TFA inhibits the binding of integrins to vitronectin, fibronectin, fibrinogen and LAP (TGF-β), and serves as an internal standard for solid-phase integrin binding assays. Cilengitide TFA inhibits tumor cell viability, induces apoptosis, reduces the phosphorylation levels of STAT3, AKT and mTOR, downregulates the expression of PD-L1, inhibits cell viability and angiogenesis, regulates anti-tumor immune responses and slows tumor growth. Cilengitide TFA can be used in research related to glioblastoma, melanoma, advanced solid tumors and refractory brain tumors .
75
75 Cited Publications
Research Areas:
CX-5461 is a selective, orally active RNA polymerase I inhibitor. CX-5461 disrupts the formation of the SL1-rDNA complex, thereby blocking the transcription initiation of ribosomal RNA without altering the activity of RNA polymerase II, DNA replication, or protein translation processes. CX-5461 upregulates the expression of p21, MDM2, Sestrin1/2, and phosphorylated AMPKα, and reduces the level of phosphorylated Akt. CX-5461 induces G2/G2/M cell cycle arrest, Autophagy, Apoptosis, and cellular senescence, and activates CHK1, CHK2, and RPA. CX-5461 can be used in research related to osteosarcoma, cervical cancer, hematologic malignancies, high-grade serous ovarian cancer, and solid tumors .
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75 Cited Publications
Cat. No.: HY-13323A
Purity: 99.41%
Research Areas:
CX-5461 dihydrochloride is a selective, orally active RNA polymerase I inhibitor. CX-5461 dihydrochloride disrupts the formation of the SL1-rDNA complex, thereby blocking the transcription initiation of ribosomal RNA without altering the activity of RNA polymerase II, DNA replication, or protein translation processes. CX-5461 dihydrochloride upregulates the expression of p21, MDM2, Sestrin1/2, and phosphorylated AMPKα, and reduces the level of phosphorylated Akt. CX-5461 dihydrochloride induces G2/G2/M cell cycle arrest, Autophagy, Apoptosis, and cellular senescence, and activates CHK1, CHK2, and RPA. CX-5461 dihydrochloride can be used in research related to osteosarcoma, cervical cancer, hematologic malignancies, high-grade serous ovarian cancer, and solid tumors .
74
Target:
Research Areas:
Exendin‑4 (Exenatide) is an orally active, blood-brain barrier-permeable glucagon-like peptide-1 receptor (GLP‑1 receptor) agonist that resists degradation mediated by dipeptidyl peptidase IV. Exendin‑4 mediates multiple glucose-regulating effects, including stimulation of glucose-dependent insulin secretion, inhibition of glucagon production, increase in β-cell mass, delay of gastric emptying, reduction of food intake, improvement of peripheral insulin sensitivity, and restoration of normal islet structure. Exendin‑4 inhibits oxidative stress, alleviates inflammatory responses, and reduces neuronal apoptosis. Exendin‑4 reduces the aggregation level of mutant huntingtin, improves motor function, prolongs survival time, and regulates the expression levels of leptin and ghrelin. Exendin‑4 can be used in research related to type 2 diabetes, acute ischemic stroke, and Huntington's disease .
74
74 Cited Publications
Synonyms: Exenatide acetate
Target:
Research Areas:
Exendin-4 acetate (Exenatide acetate) is an orally active, blood-brain barrier-permeable glucagon-like peptide-1 receptor (GLP‑1 receptor) agonist that resists degradation mediated by dipeptidyl peptidase IV. Exendin-4 acetate mediates multiple glucose-regulating effects, including stimulation of glucose-dependent insulin secretion, inhibition of glucagon production, increase in β-cell mass, delay of gastric emptying, reduction of food intake, improvement of peripheral insulin sensitivity, and restoration of normal islet structure. Exendin-4 acetate inhibits oxidative stress, alleviates inflammatory responses, and reduces neuronal apoptosis. Exendin-4 acetate reduces the aggregation level of mutant huntingtin, improves motor function, prolongs survival time, and regulates the expression levels of leptin and ghrelin. Exendin-4 acetate can be used in research related to type 2 diabetes, acute ischemic stroke, and Huntington's disease .
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72 Cited Publications
Synonyms: Zn(II)-protoporphyrin IX; ZnPP; Zinc Protoporphyrin-9
69
Daporinad (FK866) is a non-competitive inhibitor of nicotinamide phosphoribosyltransferase (Nampt), with a Ki value of 0.3 nM. Daporinad depletes NAD+ and ATP levels, inhibits mTORC1 and MAPK/ERK pathways, and activates TFEB to induce autophagy. Daporinad causes the depletion of the endoplasmic reticulum Ca²⁺ pool, ultimately weakening the mitogen-induced Ca²⁺ signal and the activation and function of T cells. Daporinad induces cell cycle arrest and apoptosis, and inhibits cell proliferation. Daporinad can be used for the study of myeloma, liver cancer, and immunosuppression .
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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 .
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61 Cited Publications
Cat. No.: HY-B0356B
CAS No.: 86393-32-0
Synonyms: Bay-09867 hydrochloride monohydrate
Ciprofloxacin (Bay-09867) hydrochloride monohydrate is an orally active, blood-brain barrier permeable fluoroquinolone antibacterial agent. Ciprofloxacin hydrochloride monohydrate exerts bactericidal effects primarily by inhibiting topoisomerase II and IV. Ciprofloxacin hydrochloride monohydrate 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 hydrochloride monohydrate 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 hydrochloride monohydrate can be applied to research related to infections of necrotic young permanent teeth and neurotoxicity .
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
