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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
2412 Results for "
decrease
" in MedChemExpress (MCE) Product Catalog:
Products (2412)
2412 Results for "decrease" in MCE Product Catalog:
Cat. No.: HY-W758414
Target:
Isotope-Labeled Compounds Insecticide Cholinesterase (ChE) Cytochrome P450 Autophagy Reactive Oxygen Species (ROS) Apoptosis Bcl-2 Family Caspase COX Keap1-Nrf2 TNF Receptor Interleukin Related Bacterial
Research Areas:
Phoxim-d5 (phenyl-d5) (mixture of isomers) is the deuterated-labeled Phoxim (HY-B0819). Phoxim is an organophosphorus pesticide and an orally active inhibitor of cholinesterase and CYP3A, which induces neurotoxicity in Caenorhabditis elegans and causes nephrotoxicity characterized by glomerular atrophy and interstitial fibrosis. Phoxim induces inhibition of the autophagy pathway. Phoxim induces dopaminergic neuron degeneration and exacerbates Aβ-induced paralysis. Phoxim damages enterocytes and disrupts intestinal barrier integrity. Phoxim induces ROS accumulation. Phoxim induces mitochondrial apoptosis, involving upregulation of Bad, Bax, caspase-3, and caspase-9 and downregulation of Bcl-2. Phoxim inhibits mitochondrial functional enzymes (COX, Ca 2+-Mg 2+-ATPase, SDH). Phoxim upregulates Nrf2 mRNA expression in the jejunal mucosa. Phoxim increases TNF-α and decreases IL-6 and IL-8 in the intestinal mucosa. Phoxim alters gut microbial composition by increasing total bacteria and Escherichia coli and reducing Lactobacillus. Phoxim enhances energy metabolism in silver carp by upregulating key glycolytic and gluconeogenic enzymes. Phoxim is used in research on neurodegenerative diseases, nephrotoxicity, intestinal oxidative stress and barrier dysfunction, and bacterial sepsis .
Cat. No.: HY-Y1269H
CAS No.: 12125-02-9
Synonyms: Salmiac, meets analytical specification of Ph. Eur. BP USP FCC
Target:
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Ammonium chloride, meets analytical specification of Ph. Eur. BP USP FCC (Salmiac, meets analytical specification of Ph. Eur. BP USP FCC) is an inhibitor of Slc26a4 and SMAD2. Ammonium chloride, meets analytical specification of Ph. Eur. BP USP FCC reduces the protein expression level of Slc26a4 in lung tissue, and attenuates ozone-induced increases in proinflammatory cytokines, inflammatory cells, pulmonary resistance, goblet cell hyperplasia, peribronchial inflammation and thiocyanate levels in mouse tissues and bronchoalveolar lavage fluid. Ammonium chloride, meets analytical specification of Ph. Eur. BP USP FCC decreases the level of phosphorylated SMAD2, inhibits autophagy by reducing autophagy-related proteins, and enhances Cisplatin (HY-17394)-induced cancer cell apoptosis and DNA double-strand breaks. Ammonium chloride, meets analytical specification of Ph. Eur. BP USP FCC also inhibits the TCA cycle, reduces ATP production, increases glucose utilization, regulates the levels of lactic acid, glutamic acid and ATP, and induces morphological degeneration of neuroblastoma cells. Ammonium chloride, meets analytical specification of Ph. Eur. BP USP FCC can be used in studies related to ozone-induced airway injury, hepatocellular carcinoma, human cervical cancer, hepatic encephalopathy, Reye syndrome, epilepsy and neurodegenerative diseases .
Synonyms: (9S,13R)-12-OPDA
Cat. No.: HY-173119
Research Areas:
SKLB-D18 is an orally active ERK1/2/ERK5 inhibitor, with an IC50 of 38.69 nM and a Kd of 126.9 nM against human ERK1, an IC50 of 40.12 nM and a Kd of 209.8 nM against ERK2, and an IC50 of 59.72 nM and a Kd of 468.2 nM against ERK5. SKLB-D18 inhibits cancer cell proliferation, induces G0/G1 cell cycle arrest and apoptosis. SKLB-D18 reduces the levels of p-ERK5, p-RSKp90, p-c-Myc and c-Myc, and upregulates the level of p-ERK1/2, thereby inhibiting the ERK1/2/5 pathway in cells. SKLB-D18 increases LC3B-II accumulation, and decreases the levels of p62, p-mTOR and p-p70S6K. SKLB-D18 elevates the levels of ROS, lipid peroxidation and free ferrous ions, reduces the levels of NCOA4 and GPX4, and induces ferritin autophagy-dependent ferroptosis in cancer cells. SKLB-D18 exhibits antitumor activity in a triple-negative breast cancer xenograft mouse model. SKLB-D18 can be used in research related to triple-negative breast cancer .
Cat. No.: HY-179427
Research Areas:
NSD2/H3K36me2 modulator-1 is an orally active NSD2/H3K36me2 modulator. NSD2/H3K36me2 modulator-1 competitively binds to the SAM pocket of NSD2, potently inhibits NSD2 expression and suppresses H3K36me2 methylation. NSD2/H3K36me2 modulator-1 reverses epithelial-mesenchymal transition (EMT), inhibits cell migration, and induces G0/G1 phase arrest and apoptosis. NSD2/H3K36me2 modulator-1 induces decreased Mitochondrial membrane potential (MMP) and subsequent Reactive oxygen species (ROS) generation. NSD2/H3K36me2 modulator-1 can be used to research the NSD2-targeting epigenetic anticancer strategies for hepatocellular carcinoma (HCC) .
Cat. No.: HY-184926
Target:
LYTACs Asialoglycoprotein Receptor (ASGPR) Monocarboxylate Transporter Mitochondrial Metabolism MMP Cadherin
Research Areas:
PEG9MA10-PAB10-GalMA10 is a CD147 LYTAC degrader. PEG9MA10-PAB10-GalMA10 binds to the asialoglycoprotein receptor (ASGPR) via its galactose methacrylate domain, mediating its uptake by hepatoma cells. PEG9MA10-PAB10-GalMA10 induces lysosome-dependent degradation of CD147, resulting in concurrent loss of associated MCT1 and MCT4. PEG9MA10-PAB10-GalMA10 reduces extracellular lactate levels, increases intracellular lactate accumulation, inhibits glycolytic activity, and enhances mitochondrial respiratory capacity. PEG9MA10-PAB10-GalMA10 decreases the secretion of MMP-2 and MMP-9, and upregulates the expression of E-cadherin. PEG9MA10-PAB10-GalMA10 exhibits anti-tumor efficacy in hepatoma models. PEG9MA10-PAB10-GalMA10 can be used for research on liver cancer (hepatocellular carcinoma) .
Gradient elution with sodium acetate buffer-ACN eluent on two ZIC-HILIC homemade columns separates 2-deoxyuridine in under 9 min .
In Vivo:2'-Deoxyuridine (34.42 ng/mL, gavage, 15 min) passes the blood-brain barrier (BBB) to enter the hippocampus of mice brain . 2'-Deoxyuridine (20 mg/kg, gavage, daily for 4 weeks) improves cognition and memory loss and attenuates the damage to the hippocampus in Aβ25-35-induced mice model .
Cat. No.: HY-P990252
Target:
Research Areas:
Cat. No.: HY-D3103
CAS No.: 1027058-07-6
Target:
Research Areas:
CMTDP is a Fluorescent probe for detecting local polarity changes around the Cys34 domain of bovine serum albumin during pH-induced N→B conformational transition. It is a thiol-specific and polarity-sensitive probe; it covalently labels the free cysteine residue at position 34 (Cys34) of bovine serum albumin, and its fluorescence maximum emission wavelength shifts in response to solvent polarity, but not to pH and temperature. When labeled to BSA, as the local polarity around the Cys34 domain increases with rising pH, the probe shows a bathchromic shift in fluorescence emission wavelength and a decrease in fluorescence intensity, which allows quantification of the local polarity change via the relationship between emission wavelength shift and dielectric constant. CMTDP itself has absorption peaks at ~392 and 508 nm, and CMTDP-labeled BSA has excitation maxima at 376 and 470 nm at pH 6.0, with the shorter-wavelength excitation peak red-shifting as pH increases while the longer one remains stable; when excited at 470 nm, the fluorescence emission maximum shifts from 570 nm at pH 6.0 to 577 nm at pH 9.1, while free CMTDP at pH 7.4 has an emission maximum at 621 nm. The excitation/emission wavelengths for CMTDP-labeled BSA are Ex/Em = 376/570 nm at pH 6.0, Ex/Em = ~376+/573 nm at pH 7.4, Ex/Em = ~376+/575 nm at pH 8.0, Ex/Em = ~376+/577 nm at pH 9.1, and for free CMTDP at pH 7.4, Ex/Em (when excited at 470 nm) = 470/621 nm[1].
Cat. No.: HY-L040
1,192 compounds
Diabetes mellitus, usually called diabetes, is a group of metabolic disorders characterized by a high blood sugar level over a prolonged period of time. The most common types are Type I and Type II. Type I diabetes (T1D), also called juvenile onset diabetes mellitus or insulin-dependent diabetes mellitus, is characterized by destruction of the β-cells of the pancreas and insulin is not produced, whereas type II diabetes (T2D), also called non-insulin-dependent diabetes mellitus, is characterized by a progressive impairment of insulin secretion and relative decreased sensitivity of target tissues to the action of this hormone. Type 2 diabetes accounts for the vast majority of all diabetes mellitus. Diabetes of all types can lead to complications in many parts of the body and can increase the overall risk of dying prematurely. Possible complications include kidney failure, leg amputation, vision loss and nerve damage.
The pathogenesis of diabetes is complicated, and development of the safe and effective drugs against diabetes is full of challenge. Increasing studies have confirmed that the pathogenesis of diabetes is related to various signaling pathways, such as insulin signaling pathway, AMPK pathway, PPAR regulation and chromatin modification pathways. These signaling pathways have thus become the major source of the promising novel drug targets to treat metabolic diseases and diabetes.
MCE Anti-diabetic Compound Library owns a unique collection of 1,192 compounds, which mainly target SGLT, PPAR, DPP-4, AMPK, Dipeptidyl Peptidase, Glucagon Receptor, etc. This library is a useful tool for discovery anti-diabetes drugs.
Cat. No.: HY-D3117
CAS No.: 2146114-18-1
Target:
Research Areas:
MBCB is a two-photon Fluorescent probe for dual-detection of mitochondrial SO₂ derivatives and viscosity. For SO₂ derivatives detection, the probe utilizes a Michael addition mechanism: nucleophilic addition of SO₂ derivatives to the C=C bond between the carbazole skeleton and 3-methylbenzothiazolium moiety destroys the strong intramolecular charge transfer (ICT) system between these groups, while enhancing the weak ICT system between the benzothiazole group and carbazole framework; this causes the red emission at 600 nm to decrease and the blue emission at 434 nm to increase, creating a ratiometric response based on the I₄₃₄ₙₘ/I₆₀₀ₙₘ intensity ratio. For viscosity detection, in low-viscosity environments, steric hindrance creates a twisted ICT (TICT) system with weak fluorescence, while in high-viscosity environments, intramolecular rotation is blocked, the TICT state is disrupted, and the strong ICT system is recovered, leading to a strong red emission at 567 nm with negligible change to the short-wavelength emission at 415 nm, creating a ratiometric response based on the I₅₆₇ₙₘ/I₄₁₅ₙₘ intensity ratio that has a logarithmic linear relationship with viscosity. The probe has excitation/emission wavelengths of Ex/Em = 351/434, 600 nm for SO₂ derivatives detection and Ex/Em = 351/567 nm for viscosity detection, with two-photon excitation at 740 nm for bioimaging; it also exhibits good mitochondrial targeting ability with a Pearson's colocalization coefficient of 0.93 when paired with Mito-Tracker Green. The probe shows high sensitivity and selectivity for SO₂ derivatives, has low cell cytotoxicity, and can be applied to detect exogenous/endogenous HSO₃⁻ in living cells and in vivo, as well as visualize mitochondrial viscosity changes induced by nystatin[1].
Cat. No.: HY-118828AS
CAS No.: 2692624-08-9
Synonyms: (9S,13R)-12-OPDA-d5
Target:
Isotope-Labeled Compounds Lipoxygenase PGE synthase Keap1-Nrf2 IKK NF-κB NO Synthase Interleukin Related
Research Areas:
(9S,13R)-12-Oxo phytodienoic acid-d5 ((9S,13R)-12-OPDA-d5) is the deuterated-labeled (9S,13R)-12-Oxo phytodienoic acid (HY-118828A). (9S,13R)-12-Oxo phytodienoic acid ((9S,13R)-12-OPDA) is a mPGES-1 inhibitor and Nrf2 activator. (9S,13R)-12-Oxo phytodienoic acid selectively inhibits mPGES-1 expression and reduces inducible PGE2 production without affecting COX-1 or COX-2. (9S,13R)-12-Oxo phytodienoic acid inhibits the phosphorylation of IKKβ, IκBα, and NF-κB (p65), blocks the nuclear translocation of p65, increases the nuclear translocation of Nrf2, and upregulates HO-1 expression. (9S,13R)-12-Oxo phytodienoic acid inhibits the differentiation of M0 macrophages toward the M1 phenotype and promotes differentiation toward the M2 phenotype. (9S,13R)-12-Oxo phytodienoic acid decreases the levels of NO, PGE2, IL-1β, IL-6, iNOS, and PGD2. (9S,13R)-12-Oxo phytodienoic acid can be used for inflammation research .
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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
