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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
2408 Results for "
decrease
" in MedChemExpress (MCE) Product Catalog:
Products (2408)
2408 Results for "decrease" in MCE Product Catalog:
Cat. No.: HY-N18667
CAS No.: 84696-21-9
Category:
Target:
Cat. No.: HY-N1989
CAS No.: 11028-00-5
Cat. No.: HY-N2492R
CAS No.: 19367-38-5
Synonyms: Methyl trans-p-coumarate (Standard)
Category:
Leguminosae/Fabaceae Extract Plant Flavonoids Flavones Glycyrrhiza uralensis Fisch. Extract Phenols Polyphenols
Target:
Cat. No.: HY-P10159
CAS No.: 1809102-71-3
Target:
Research Areas:
DJK-5 is an antimicrobial peptide that targets and degrades guanosine pentaphosphate and tetraphosphate (pppGpp and ppGpp). DJK-5 kills bacteria within dentinal tubules, dental plaque and preformed oral biofilms, delays biofilm recovery, reduces the abundance of extracellular polysaccharides and the structural integrity of biofilm matrices, and inhibits the formation and biomass accumulation of dental plaque biofilms. DJK-5 permeabilizes bacterial membranes, induces bacterial morphological changes, inhibits bacterial growth, and exerts a synergistic effect on bacterial biofilms when used in combination with traditional antibiotics and Colistin (HY-113678). DJK-5 exhibits protease resistance and broad-spectrum antibiofilm activity, though its activity decreases in fetal bovine serum. DJK-5 can be used in studies of pulpitis, mixed biofilm infections, skin abscesses, dental caries, infections associated with failed root canal therapy, and Pseudomonas aeruginosa biofilm-related respiratory tract infections .
Cat. No.: HY-P5142
CAS No.: 193981-10-1
Synonyms: ω-ACTX-Hv1; ω-Atracotoxin-HV1
Research Areas:
Cardiovascular Disease Neurological Disease Inflammation/Immunology
Cat. No.: HY-P5142A
Synonyms: ω-ACTX-Hv1 TFA; ω-Atracotoxin-HV1 TFA
Research Areas:
Cardiovascular Disease Neurological Disease Inflammation/Immunology
Cat. No.: HY-W014937
CAS No.: 1137-42-4
Synonyms: 4HBP
Target:
Drug Metabolite PERK Eukaryotic Initiation Factor (eIF) NF-κB TNF Receptor Interleukin Related Reactive Oxygen Species (ROS) Apoptosis
Research Areas:
4‑Hydroxybenzophenone (4HBP) is a major metabolite of Benzophenone (HY-Y0546) and is orally active. 4-Hydroxybenzophenone triggers endoplasmic reticulum stress and activates the PERK-eIF2α-ATF4-CHOP and IRE1α-XBP1s pathways, and inhibits IκB translation. 4-Hydroxybenzophenone induces endoplasmic reticulum stress, unfolded protein response activation, protein homeostasis imbalance, protein aggregation, oxidative stress, ROS accumulation, mitochondrial membrane potential decrease, ATP depletion, and cytotoxicity. 4-Hydroxybenzophenone induces neural stem cell apoptosis (apoptosis) and affects neuronal differentiation. 4-Hydroxybenzophenone promotes malignant proliferation of hepatocellular carcinoma cells and xenograft tumor growth in nude mice. 4-Hydroxybenzophenone can be used in research related to neurodevelopmental toxicity and hepatocellular carcinoma .
Cat. No.: HY-W015551
CAS No.: 3913-81-3
Synonyms: (E)-Dec-2-enal
Cat. No.: HY-W017087
CAS No.: 135-77-3
Research Areas:
1,2,4-Trimethoxybenzene is an orally active NLRP3 selective inhibitor. 1,2,4-Trimethoxybenzene can markedly suppress Nigericin (HY-127019) or ATP (HY-B2176)-induced NLRP3 inflammasome activation, thus decreasing caspase-1 activation and IL-1β secretion. 1,2,4-Trimethoxybenzene specifically inhibits the activation of NLRP3 inflammasome without affecting absent in melanoma 2 (AIM2) inflammasome activation. 1,2,4-Trimethoxybenzene inhibits oligomerization of the apoptosis-associated speck-like protein containing a CARD (ASC) and protein-protein interaction between NLRP3 and ASC, thus blocking NLRP3 inflammasome assembly. 1,2,4-Trimethoxybenzene can be used for the study of experimental autoimmune encephalomyelitis (EAE), multiple sclerosis, and type 2 diabetes .
Cat. No.: HY-W048513
CAS No.: 60129-59-1
Cat. No.: HY-W062109S
CAS No.: 1231979-85-3
Cat. No.: HY-W089800
CAS No.: 18829-56-6
Synonyms: trans-2-Nonen-1-al
Target:
Research Areas:
trans-2-Nonenal (trans-2-Nonen-1-al) is an endogenous peroxidation product of polyunsaturated fatty acids, acting as an inhibitor of COX and 12-LOX, as well as an inducer of apoptosis. trans-2-Nonenal is also a malodorous compound secreted by the human body, and its content gradually increases with aging. trans-2-Nonenal inhibits the activities of multiple enzymes such as platelet membrane-bound PTPase, preferentially covalently modifies proteins at lysine residues to form immunogenic adducts, and regulates platelet Arachidonic acid (HY-109590) metabolism. trans-2-Nonenal also exhibits significant cytotoxicity, reduces the viability of keratinocytes, promotes their apoptosis, and effectively decreases the thickness of epidermal models and the number of proliferating cells. trans-2-Nonenal is commonly used in studies of thrombotic, atherosclerotic diseases, renal adenocarcinoma, etc. .
Cat. No.: HY-W1015419
CAS No.: 73804-75-8
Synonyms: α-Fluoromethylhistidine
Target:
Research Areas:
α-FMH (α-Fluoromethylhistidine) is an orally active histidine decarboxylase inhibitor. α-FMH depletes histamine in enterochromaffin-like (ECL) cells, reduces the number and volume density of secretory vesicles in ECL cells, and does not affect histamine storage in mast cells. α-FMH abolishes Omeprazole (HY-B0113)-induced vacuolization of ECL cells and decreases gastrin-induced histamine efflux from ECL cells. α-FMH does not alter the granular characteristics of ECL cells, omeprazole-induced hypertrophy of ECL cells, gastrin-induced pancreastatin-like immunoreactivity efflux, nor does it affect gastric acid secretion induced by histamine or vagal stimulation. α-FMH inhibits basal and gastrin-stimulated gastric acid secretion, reduces acid output induced by gastrin+IBMX (HY-12318), but does not directly affect acid generation in isolated parietal cells .
Cat. No.: HY-W777360
CAS No.: 1189461-56-0
Cat. No.: HY-L169
722 compounds
Resistance refers to the decrease in the effectiveness of drugs in treating diseases or symptoms. Due to the increasing global antibiotic resistance, it may threaten our ability to treat common infectious diseases. Drug resistance is also the main cause of chemotherapy failure in malignant tumors. In approximately 50% of cases, drug resistance exists even before chemotherapy begins. There are many mechanisms of anticancer drug resistance, including increased protein expression that leads to drug removal, mutations in drug binding sites, recovery of tumor protein production, and pre-existing genetic heterogeneity in tumor cell populations. In addition, the issue of drug resistance seems to have affected the development of new anticancer drugs. Drug resistance may be caused by various conditions, such as mutations, epigenetic modifications, and upregulation of drug efflux protein expression. Overcoming multidrug resistance in cancer treatment is becoming increasingly important.
MCE designs a unique collection of 722 anti-drug-resistant compounds. It is a good tool to be used for research on cancer and other diseases.
Cat. No.: HY-100742R
CAS No.: 1802977-61-2
GNE-140 racemate (Standard) is the analytical standard of GNE-140 racemate (HY-100742). This product is intended for research and analytical applications. GNE-140 racemate is a racemic mixture of (R)-GNE-140 (HY-100742A) and (S)-GNE-140 (HY-100742B), and also a tautomer of GNE-140 (HY-118241). GNE-140 racemate is an orally active lactate dehydrogenase inhibitor, with an IC50 of 3 nM against human LDHA and an IC50 of 5 nM against LDHB. GNE-140 racemate reduces the phosphorylation level and total protein expression of p38 MAPK, and inhibits EGF-induced AKT phosphorylation. GNE-140 racemate decreases lactate production, regulates glycolysis, the pentose phosphate pathway and nucleotide biosynthesis, increases extracellular pH, inhibits cell proliferation, migration and invasion, and induces caspase-3 activation and ROS accumulation. GNE-140 racemate can be used in research related to breast cancer, cystic fibrosis and pancreatic cancer .
Cat. No.: HY-100977S
CAS No.: 3006902-95-7
Synonyms: DiMC-d6; CHC 004-d6; Di-O-methylcurcumin-d6
Target:
Isotope-Labeled Compounds Androgen Receptor Reactive Oxygen Species (ROS) Apoptosis NF-κB CDK Fatty Acid Synthase (FASN) Acetyl-CoA Carboxylase PI3K Akt AMPK ERK JNK
Research Areas:
Dimethoxycurcumin-d6 (DiMC-d6; CHC 004-d6; Di-O-methylcurcumin-d6) is the deuterated-labeled Dimethoxycurcumin (HY-100977). Dimethoxycurcumin (DiMC) is a curcuminoid compound found in Curcuma longa. Dimethoxycurcumin is also an orally active thioredoxin reductase inhibitor (IC50 = 5.4 μM) and androgen receptor antagonist. Dimethoxycurcumin inhibits thioredoxin reductase, leading to oxidized thioredoxin accumulation, ROS production, DNA damage, glutathione depletion, mitochondrial membrane potential decrease, ATP depletion, S phase arrest, and apoptosis. Dimethoxycurcumin inhibits NF-κB, NADPH oxidase subunits, ATP synthase subunits, CDK4, cyclin-D1, FASN, ACC, and the IRS2-PI3K-Akt pathway, while activating AMPK, ERK, and JNK. Dimethoxycurcumin can be used for research on cancer, arsenic-induced hepatotoxicity, and tuberculosis .
Cat. No.: HY-102093A
CAS No.: 151801-76-2
ZD 7155 is an AT1R selective antagonist with renal function modulating activity. The effects of ZD 7155 on glomeruli and tubules were measured in 1- (N = 9) and 6-week-old (N = 13) lambs. Pretreatment with ZD 7155 after L-NAME infusion did not alter glomerular function in 1- or 6-week-old lambs. During postnatal development, Ang II modulates the effects of NO on electrolyte handling via AT1R and AT2R. In 6-week-old lambs, selective inhibition of AT1R and AT2R increased the excretion of Na+, K+, and Cl-. In 6-week-old lambs, pretreatment with ZD 7155 and PD 123319 followed by the addition of L-NAME increased urine flow rate by 200%, free water clearance by 50%, and decreased urine osmolality by 40%. The same trends of changes in these variables were also observed when L-NAME was added to ZD 7155 or PD 123319, although to a lesser extent.
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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
