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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
13 Results for "
membrane damage response
" in MedChemExpress (MCE) Product Catalog:
Products (13)
13 Results for "membrane damage response" in MCE Product Catalog:
11
Target:
Research Areas:
Elrelesertib (AZD1390) is an orally active, brain-penetrant ATM kinase inhibitor with IC50 values of 0.78 nM. Elrelesertib blocks ATM-dependent DNA damage response, inhibits ATM autophosphorylation and downstream Chk2, Rad50 phosphorylation, and accumulates at DNA breaks. Elrelesertib acts as a radiosensitizer, induces apoptosis, genomic instability, G2-M cell cycle arrest, ROS elevation, and mitochondrial membrane potential alteration. Elrelesertib has low efflux liability against P-gp and BCRP. Elrelesertib can be used for the research of central nervous system malignancies, glioblastoma multiforme, glioma, lung cancer brain metastases, and breast cancer .
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1 Cited Publications
Cat. No.: HY-N9447
CAS No.: 79595-97-4
Category:
Cat. No.: HY-P10408
CAS No.: 1906866-53-2
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Cat. No.: HY-B0871
CAS No.: 84087-01-4
Research Areas:
Quinclorac is a highly selective quinoline carboxylic acid synthetic auxin herbicide. Quinclorac weakly inhibits HPPD, accompanied by a transient decrease in carotenoids. Quinclorac upregulates ACC synthase (ACS), leading to the co-accumulation of ethylene and cyanide, while increasing the ABA/IAA ratio, which induces ROS burst, membrane lipid peroxidation (MDA) and lethal growth inhibition. Residual Quinclorac in soil can cause abnormal growth of subsequent tobacco crops. In calli of Phaseolus vulgaris, Quinclorac induces oxidative stress (increased MDA and decreased RGR), but cells after stepwise pressurized acclimation acquire a constitutive antioxidant state, which remains stable after de-acclimation and tolerates oxidative damage caused by Quinclorac. Quinclorac can be used in studies related to herbicide action mechanisms, bioremediation of soil residues, and adaptive responses of plant cells to oxidative stress .
Cat. No.: HY-N16657
CAS No.: 189757-88-8
Synonyms: LI-F 04b
Category:
Cat. No.: HY-171936
CAS No.: 1329115-44-7
Synonyms: GM1 (d18:1/C18:0) ammonium; C18 Ganglioside GM1 (d18:1/18:0) ammonium
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Ganglioside GM1 (ammonium) is a monosialylated ganglioside and the prototypic ganglioside for those containing one sialic acid residue. Ganglioside GM1 (ammonium) is one of the most abundant gangliosides in the brain which provides neuroprotection. Ganglioside GM1 (ammonium) exhibits anti-inflammatory property. Ganglioside GM1 (ammonium) has a well-balanced amphiphilic behavior. Ganglioside GM1 (ammonium) can reduce the fluidity of the plasma membrane that implies a retention and enrichment of the ganglioside in specific membrane domains that are called lipid rafts. Ganglioside GM1 (ammonium) can modify the process of differentiation, amplifies responses to neurotrophic factors, protects against excitatory amino acid-related neurotoxicity. Ganglioside GM1 (ammonium) can alleviate acute nerve cell damage through blocking cytotoxicity and potentiating neurotophic factors. Ganglioside GM1 (ammonium) can be studied in neurodegenerative diseases such as Alzheimer’s disease .
Cat. No.: HY-183781
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Research Areas:
RIPK1-IN-41 is an orally active RIPK1 inhibitor with an IC50 of 92 nM and a KD of 106.8 nM. RIPK1-IN-41 reduces the phosphorylation level of RIPK1, inhibits necrosome formation, blocks the activation of RIPK3 and MLKL, maintains mitochondrial and lysosomal functions, preserves cell membrane integrity, and suppresses necroptosis. RIPK1-IN-41 alleviates hypothermia and multi-organ damage in a mouse model of systemic inflammatory response syndrome induced by mTNF-α. RIPK1-IN-41 is applicable to research related to systemic inflammatory response syndrome .
Cat. No.: HY-182586
CAS No.: 19198-75-5
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Research Areas:
Decyl gallate is an antifungal (fungal) agent. Decyl gallate downregulates the expression of the pro-apoptotic (apoptosis) protein Bak, upregulates the expression of the anti-apoptotic protein Bcl-2, and inhibits DNA damage. Decyl gallate disrupts ALG12-mediated N-glycosylation, overactivates the UPR pathway, and simultaneously reduces fungal cell wall enzyme activity, chitin levels, mitochondrial activity, budding ability, cell viability, and host cell adhesion capacity. Decyl gallate reduces inflammatory responses induced by fungal infection and disrupts fungal membrane structure. Decyl gallate can be used in studies related to paracoccidioidomycosis and invasive fungal infections .
Cat. No.: HY-109566R
CAS No.: 2089288-03-7
Synonyms: AZD1390 (Standard)
Research Areas:
Elrelesertib (Standard) (AZD1390 (Standard)) is the analytical standard of Elrelesertib (AZD1390) (HY-109566). This product is intended for research and analytical applications. Elrelesertib (AZD1390) is an orally active, brain-penetrant ATM kinase inhibitor with IC50 values of 0.78 nM. Elrelesertib blocks ATM-dependent DNA damage response, inhibits ATM autophosphorylation and downstream Chk2, Rad50 phosphorylation, and accumulates at DNA breaks. Elrelesertib acts as a radiosensitizer, induces apoptosis, genomic instability, G2-M cell cycle arrest, ROS elevation, and mitochondrial membrane potential alteration. Elrelesertib has low efflux liability against P-gp and BCRP. Elrelesertib can be used for the research of central nervous system malignancies, glioblastoma multiforme, glioma, lung cancer brain metastases, and breast cancer .
Cat. No.: HY-P11580
Target:
Research Areas:
Cat. No.: HY-B0871R
CAS No.: 84087-01-4
Research Areas:
Quinclorac (Standard) is the analytical standard of Quinclorac (HY-B0871). This product is intended for research and analytical applications. Quinclorac is a highly selective quinoline carboxylic acid synthetic auxin herbicide. Quinclorac weakly inhibits HPPD, accompanied by a transient decrease in carotenoids. Quinclorac upregulates ACC synthase (ACS), leading to the co-accumulation of ethylene and cyanide, while increasing the ABA/IAA ratio, which induces ROS burst, membrane lipid peroxidation (MDA) and lethal growth inhibition. Residual Quinclorac in soil can cause abnormal growth of subsequent tobacco crops. In calli of Phaseolus vulgaris, Quinclorac induces oxidative stress (increased MDA and decreased RGR), but cells after stepwise pressurized acclimation acquire a constitutive antioxidant state, which remains stable after de-acclimation and tolerates oxidative damage caused by Quinclorac. Quinclorac can be used in studies related to herbicide action mechanisms, bioremediation of soil residues, and adaptive responses of plant cells to oxidative stress .
Cat. No.: HY-B0871S
Research Areas:
Quinclorac- 13C is the 13C-labeled Quinclorac (HY-B0871). Quinclorac is a highly selective quinoline carboxylic acid synthetic auxin herbicide. Quinclorac weakly inhibits HPPD, accompanied by a transient decrease in carotenoids. Quinclorac upregulates ACC synthase (ACS), leading to the co-accumulation of ethylene and cyanide, while increasing the ABA/IAA ratio, which induces ROS burst, membrane lipid peroxidation (MDA) and lethal growth inhibition. Residual Quinclorac in soil can cause abnormal growth of subsequent tobacco crops. In calli of Phaseolus vulgaris, Quinclorac induces oxidative stress (increased MDA and decreased RGR), but cells after stepwise pressurized acclimation acquire a constitutive antioxidant state, which remains stable after de-acclimation and tolerates oxidative damage caused by Quinclorac. Quinclorac can be used in studies related to herbicide action mechanisms, bioremediation of soil residues, and adaptive responses of plant cells to oxidative stress .
Cat. No.: HY-W715812
CAS No.: 116255-48-2
Target:
Fungal Apoptosis Caspase Reactive Oxygen Species (ROS) MDM-2/p53 SOD Bcl-2 Family PERK JNK p38 MAPK
Research Areas:
Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability . Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process . Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction .
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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
