641 Results for "

Systemic

" in MedChemExpress (MCE) Product Catalog:
Products (641)

641 Results for "Systemic" in MCE Product Catalog:

Cat. No.: HY-10071R
CAS No.: 146986-50-7
Y-27632 (Standard) is the analytical standard of Y-27632 (HY-10071). This product is intended for research and analytical applications. Y-27632 is a ROCK inhibitor with Ki values of 220 nM and 300 nM for ROCK1 and ROCK2, respectively. Y-27632 exerts anti-inflammatory and immunomodulatory effects in systemic lupus erythematosus models by inhibiting the ROCK/NF-κB pathway. Y-27632 enhances autophagy by inhibiting the AKT/mTOR pathway, thereby inducing apoptosis apoptosis in oral squamous cell carcinoma. Y-27632 induces the formation of tunneling nanotubes in ARPE-19 cells and significantly enhances mitochondrial transfer through these channels. Y-27632 promotes neurite outgrowth in PC12 cells by activating the Rac1/NOX1/ROS/AKT/PAK1 signaling cascade .
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Cat. No.: HY-14519AR
CAS No.: 7413-34-5
Synonyms: Amethopterin disodium (Standard); CL14377 disodium (Standard); WR19039 disodium (Standard)
Methotrexate disodium (Standard) (Amethopterin disodium (Standard); CL14377 disodium (Standard); WR19039 disodium (Standard)) is the analytical standard of Methotrexate disodium (HY-14519A). This product is intended for research and analytical applications. Methotrexate disodium (Amethopterin disodium; CL14377 disodium; WR19039 disodium) is an orally active antifolate (Antifolate). Methotrexate disodium inhibits dihydrofolate reductase (DHFR), blocks tetrahydrofolate production, suppresses purine/pyrimidine synthesis and transmethylation, and causes intracellular accumulation of AICAR. Methotrexate disodium promotes extracellular adenosine release, regulates the cytokine network, and inhibits the alarmin function of HMGB1. Methotrexate disodium induces apoptosis and cytotoxicity, upregulates the expression of iNOS and COX-2, suppresses hippocampal neurogenesis, and induces pulmonary fibrosis. Methotrexate disodium is used in the research of various immune and inflammation-related diseases such as arthritis, psoriasis, systemic lupus erythematosus, as well as pulmonary fibrosis and breast cancer .
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Cat. No.: HY-157763
Research Areas:  

Cancer

Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1 is a cleavable linker-payload conjugate and cereblon-binding BTK bifunctional degrader. Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1 induces BTK degradation and exerts cytotoxic effects when delivered via CD79b monoclonal antibody. Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1, when formulated as a CD79b antibody-drug conjugate, achieves sustained in vivo BTK degradation in tumor-bearing mice with reduced systemic payload exposure. Mal-PEG1-Val-Cit-PABC-diphosphate-BTK degrader-1 can be used for the research of activated b-cell-like diffuse large b-cell lymphoma (ADC linker: (HY-130944); PROTAC: (HY-163295)) .
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Cat. No.: HY-B1451R
CAS No.: 89396-94-1
Synonyms: TA-6366 (Standard)
Imidapril (hydrochloride) (Standard) is the analytical standard of Imidapril (hydrochloride). This product is intended for research and analytical applications. Imidapril hydrochloride (TA-6366) is an orally active dual inhibitor of angiotensin-converting enzyme (ACE) and MMP-9. Imidapril hydrochloride inhibits lipopolysaccharide-induced phosphorylation of c-Jun, MKK4 and JNK in monocytes, and downregulates the production of specific inflammatory factors such as TNF-α and IP-10, thereby exerting anti-inflammatory activity. Imidapril hydrochloride also effectively ameliorates mesangial expansion and reduces urinary albumin excretion by inhibiting angiotensin AngII production, lowering glomerular pressure and oxidative stress, thus delaying disease progression. Imidapril hydrochloride can also directly bind to the active site of MMP-9 to inhibit gelatinase activity, and suppress the enlargement of cerebral aneurysms without altering systemic blood pressure. Imidapril hydrochloride is widely applicable to related studies on autoimmune glomerulonephritis, diabetic nephropathy, cerebral aneurysms and other conditions .
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Cat. No.: HY-B1451S
CAS No.: 1356017-30-5
Imidapril-d3 hydrochloride (TA-6366-d3) is the deuterium labeled Imidapril hydrochloride. Imidapril hydrochloride (TA-6366) is an orally active dual inhibitor of angiotensin-converting enzyme (ACE) and MMP-9. Imidapril hydrochloride inhibits lipopolysaccharide-induced phosphorylation of c-Jun, MKK4 and JNK in monocytes, and downregulates the production of specific inflammatory factors such as TNF-α and IP-10, thereby exerting anti-inflammatory activity. Imidapril hydrochloride also effectively ameliorates mesangial expansion and reduces urinary albumin excretion by inhibiting angiotensin AngII production, lowering glomerular pressure and oxidative stress, thus delaying disease progression. Imidapril hydrochloride can also directly bind to the active site of MMP-9 to inhibit gelatinase activity, and suppress the enlargement of cerebral aneurysms without altering systemic blood pressure. Imidapril hydrochloride is widely applicable to related studies on autoimmune glomerulonephritis, diabetic nephropathy, cerebral aneurysms and other conditions .
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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 .
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Cat. No.: HY-L215
6,077 compounds

Metabolomics, positioned as the systemic characterization of small-molecule metabolites within biological systems, has emerged as an indispensable analytical platform in both fundamental research and translational applications across plant sciences, microbial biotechnology, and biomedical investigations. Functioning as a critical component in multi-omics integration, this discipline deciphers the intricate molecular networks operating downstream of genomic, transcriptomic, and proteomic regulation, thereby capturing the dynamic biochemical phenotype closest to organismal functionality. The metabolome, comprising endogenous compounds with molecular weights typically below 1500 Da, serves as the functional readout of cellular processes and environmental interactions, where perturbations in metabolic networks are frequently implicated in disease pathogenesis. Such unique attributes have propelled metabolomics into a pivotal role in pharmacological research, particularly in target deconvolution, pharmacodynamic assessment, and mechanistic elucidation of pathological processes.

MCE can provide 6,077 mass spectrometry human metabolites that can be used for metabolite identification and quantification, functional cell detection and phenotypic screening of mass spectrometry.

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 .
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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 .
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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 .
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Cat. No.: HY-121151S2
Synonyms: (±)-Amethopterin-13C,d3 disodium; (±)-CL14377-13C,d3 disodium; (±)-WR19039-13C,d3 disodium
(±)-Methotrexate- 13C,d3 disodium ((±)-Amethopterin- 13C,d3 disodium; (±)-CL14377- 13C,d3 disodium; (±)-WR19039- 13C,d3 disodium) is the deuterated, 13C-labeled (±)-Methotrexate (HY-121151). (±)-Methotrexate is the racemate of Methotrexate (HY-14519). Methotrexate is an orally active antifolate (Antifolate). Methotrexate inhibits dihydrofolate reductase (DHFR), blocks tetrahydrofolate production, suppresses purine/pyrimidine synthesis and transmethylation, and causes intracellular accumulation of AICAR. Methotrexate promotes extracellular adenosine release, regulates the cytokine network, and inhibits the alarmin function of HMGB1. Methotrexate induces apoptosis and cytotoxicity, upregulates the expression of iNOS and COX-2, suppresses hippocampal neurogenesis, and induces pulmonary fibrosis. Methotrexate is used in the research of various immune and inflammation-related diseases such as arthritis, psoriasis, systemic lupus erythematosus, as well as pulmonary fibrosis and breast cancer .
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Cat. No.: HY-144026S
CAS No.: 1809222-43-2
9-PAHSA-d9 is the deuterium labeled 9-PAHSA (HY-120657). 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 .
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Cat. No.: HY-164288
CAS No.: 2287331-29-5
Synonyms: TDI-006570
TDI-6570 (TDI-006570) is a blood-brain barrier-permeable, orally active cGAS inhibitor with an IC50 of 1.64 μM. TDI-6570 exhibits high gastrointestinal absorption and a long brain half-life in mice, and shows no toxicity to primary neurons. By inhibiting the cGAS-STING-IFN signaling pathway, TDI-6570 reduces STING levels and the activation of TBK1, blocks double-stranded DNA-induced cGAS activation and downstream interferon-stimulated gene expression, thereby reducing tau protein spread and improving synaptic loss. TDI-6570 reverses memory deficits, increases the amplitude of long-term potentiation, enhances the MEF2C transcriptional network, restores PSD-95 and vGAT punctate structures, and significantly improves cognitive resilience. TDI-6570 can be applied to the research of Alzheimer's disease, Parkinson's disease, systemic lupus erythematosus, as well as various central nervous system and autoimmune diseases .
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Cat. No.: HY-P990955
CAS No.: 2839652-75-2
Synonyms: ADX-097

Target:  

CD3 Complement System

Research Areas:  

Inflammation/Immunology

Ebribafusp alfa (ADX-097) comprising a humanized anti-C3d monoclonal antibody linked to two moieties of the first five consensus repeats of factor H (fH1-5). Ebribafusp alfa binds C3d and related fragments, catalyzes AP convertase dissociation, acts as a factor I co-factor for C3b cleavage, and delivers fH1-5 moieties to C3d-deposited tissues for local complement inhibition without systemic blockade. Ebribafusp alfa reduces glomerular C3 deposition, proteinuria, urine albumin-creatinine ratios, and urine soluble C5b-9 levels, preserves podocyte foot-process architecture, inhibits skin complement activation, and localizes to UVB-damaged primate skin. Ebribafusp alfa can be used for the research of membranous nephropathy, bullous pemphigoid, discoid lupus erythematosus, C3 glomerulopathy, IgA nephropathy, and lupus nephritis .
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Cat. No.: HY-P991510

Target:  

TNF Receptor

Research Areas:  

Cancer

CDX-1140 is a fully human IgG monoclonal antibody and CD40 agonist, with a Kd value of 0.01 nM against human targets. The epitope of CDX-1140 locates at CD40 CRD1 and avoids the CD40L binding site. It activates DCs and B cells, drives NF-κB reporter gene activation, exhibits agonist activity independent of FcR cross-linking, and shows a synergistic effect with recombinant CD40L . CDX-1140 does not induce systemic cytokine release, exerts direct and immune-mediated anti-tumor activity in tumor xenografts, and has favorable safety profiles. When used as a local vaccine adjuvant in combination with 6MHP+mBRAF+poly-ICLC, CDX-1140 increases the number of DC-LAMP + DCs and induces Th1 CD4 + responses in high-risk melanoma. CDX-1140 can be used in studies related to B-cell lymphoma, bladder cancer and high-risk melanoma .
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Cat. No.: HY-164919
CAS No.: 2847102-44-5
Synonyms: XMT-2056
Calotatug ginistinag (XMT-2056) is an antibody-drug conjugate (ADC) targeting HER2, linked to a payload composed of XMT-1519 conjugate-1 (HY-148067) and STING agonist-20 (HY-148068). Calotatug ginistinag activates the STING signaling pathway in tumor cells and tumor-resident immune cells, induces the production of type I interferons and cytokines (CXCL10, IFN-β, IL-6, TNF-α, triggers innate anti-tumor immune responses, and exerts a bystander effect. Calotatug ginistinag exhibits efficacy against HER2-expressing cancer cells in co-culture with PBMCs. Calotatug ginistinag induces tumor regression and reduces systemic inflammation in various tumor models. Combination treatment with Calotatug ginistinag, Trastuzumab (HY-P9907) and T-DXd (HY-138298) yields benefits. Calotatug ginistinag can be used in studies related to HER2-expressing solid tumors such as breast cancer, gastric cancer and ovarian cancer .
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Cat. No.: HY-L251
93 compounds

Ionizable lipids are a class of specialized, functional lipid molecules with pH-sensitive charge characteristics. They are primarily divided into two major categories: ionizable cationic lipids and ionizable anionic lipids, though the term typically specifies ionizable cationic lipids within the biomedical field. Structurally, these lipids consist of an ionizable hydrophilic headgroup, a biodegradable linker, and hydrophobic tails. Their primary application is serving as the key delivery vehicle in lipid nanoparticles (LNPs) to encapsulate negatively charged nucleic acid macromolecules, such as mRNA vaccines, siRNA therapeutics, and CRISPR gene-editing components. In a physiological, neutral environment, they remain electrically neutral to minimize systemic toxicity and prolong circulation time. Upon entering the acidic microenvironment of cellular endosomes, however, they undergo protonation to become positively charged, thereby inducing membrane fusion and enabling the highly efficient intracellular release of the nucleic acid cargo. Consequently, they serve as the technological cornerstone for bringing nucleic acid therapies into clinical application.

To accelerate the translational process of cutting-edge nucleic acid drugs, MCE has meticulously constructed an ionizable lipid compound library containing 93 high-performance molecules, aiming to provide researchers and pharmaceutical professionals with a high-throughput, multi-dimensional lipid screening platform.

Cat. No.: HY-L076
641 compounds

Drug-induced liver injury (DILI; also known as drug-induced hepatotoxicity) is caused by medications (prescription or OTC), herbal and dietary supplements (HDS), or other xenobiotics that result in abnormalities in liver tests or in hepatic dysfunction that cannot be explained by other causes. Drugs are an important cause of liver injury. Drug-induced hepatic injury is the most common reason cited for withdrawal of an approved drug.

DILI is thought to occur via several different mechanisms. Among these are direct impairment of the structural (e.g., mitochondrial dysfunction) and functional integrity of the liver; production of a metabolite that alters hepatocellular structure and function; production of a reactive drug metabolite that binds to hepatic proteins to produce new antigenic drug-protein adducts, which are targeted by hosts’ defenses (the hapten hypothesis); and initiation of a systemic hypersensitivity response (i.e., drug allergy) that damages the liver.

MCE Drug-induced Liver Injury (DILI) Compound Library contains a unique collection of 641 hepatotoxicity causing compounds and is a powerful tool to research DILI and other drug toxicities. This library can be used to understand the mechanisms of DILI, identify biomarkers for early DILI prediction, and allow timely recognition during drug development, thus finally achieving successful DILI prevention and assessment in the pre-marketing phase.

Cat. No.: HY-156466
CAS No.: 2848664-42-4
Purity:  99.95%
Research Areas:  

Inflammation/Immunology

QL-1200186 is a selective, orally active, allosteric inhibitor targeting the tyrosine kinase TYK2 pseudokinase domain JH2 (IC50=0.06 nM, TYK2 JH2), with 164-fold selectivity over TYK1 JH2 (IC50=9.85 nM,TYK1 JH2). QL-1200186 first stabilizes the TYK2 JH2 conformation, inhibits the activity of the JH1 catalytic domain, and blocks the IFNα, IL-12/IL-23-mediated JAK-STAT signaling pathway. QL-1200186 can inhibit the production of Th1/Th17 cell-related cytokines (such as IFNγ, IL-23), reduce immune cell activation, and has no significant effect on JAK1/2/3 kinase activity. QL-1200186 can significantly improve skin inflammation in the Imiquimod (HY-B0180)-induced psoriasis mouse model and reduce the Psoriasis Area and Severity Index (PASI) score. QL-1200186 can be used in the study of autoimmune diseases such as psoriasis and systemic lupus erythematosus (SLE) .
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Cat. No.: HY-182360
Cytisine-Platinum(IV) Prodrug-1 is a Pt(IV) prodrug incorporating the natural compound Cytisine (HY-N0175) with antiproliferative activity against tumor cells. Cytisine-Platinum(IV) Prodrug-1 promotes calcium transfer across the IP3R1-GRP75-VDAC1 axis to drive mitochondrial calcium overload. Cytisine-Platinum(IV) Prodrug-1 initiates unfolded protein response via PERK, eIF2α, ATF4, and CHOP to modulate Bcl-2 and Bax, triggering apoptosis. Cytisine-Platinum(IV) Prodrug-1 induces mitochondrial dysfunction, ROS production, reduced ATP synthesis, DNA damage, and S-phase cell cycle arrest. Cytisine-Platinum(IV) Prodrug-1 activates the cGAS-STING pathway, reduces PD-L1 expression, drives immunogenic cell death. Cytisine-Platinum(IV) Prodrug-1 exhibits high physiological stability, efficient cellular accumulation, and enhanced platinum-DNA binding, and inhibits tumor growth in mouse models with reduced systemic toxicity. Cytisine-Platinum(IV) Prodrug-1 can be used for the research of lung cancer .
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