18 Results for "

immune evasion

" in MedChemExpress (MCE) Product Catalog:
Products (18)

18 Results for "immune evasion" in MCE Product Catalog:

2
2 Cited Publications
Cat. No.: HY-162080
CAS No.: 374705-10-9
Research Areas:  

Cancer

METTL1-WDR4-IN-1 (Compound 1) is a selective competitive inhibitor of the methyltransferase complex METTL1-WDR4 (IC50 = 144 μM). METTL1-WDR4-IN-1 inhibits the m 7G methyltransferase activity of the METTL1-WDR4 complex, blocking m 7G modification of PKM mRNA, reducing PKM2 protein expression, disrupting the METTL1/PKM2/H3K9la positive feedback loop, and simultaneously inhibiting PKM2 nuclear translocation-mediated CD155 transcriptional activation. METTL1-WDR4-IN-1 can inhibit tumor cell proliferation, weaken glycolytic metabolism, reverse tumor immune evasion (restoring NK cell and CD8 + T cell function), and regulate RNA epigenetic modification and the tumor immune microenvironment. METTL1-WDR4-IN-1 can be used in immunotherapy research for cancers such as colorectal cancer, and is particularly suitable for use in combination with PKM2 inhibitors to enhance anti-tumor treatment efficacy .
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2
2 Cited Publications
Cat. No.: HY-162080A
Research Areas:  

Cancer

METTL1-WDR4-IN-1 (Compound 1) TFA is a selective competitive inhibitor of the methyltransferase complex METTL1-WDR4 (IC50=144 μM). METTL1-WDR4-IN-1 TFA inhibits the m 7G methyltransferase activity of the METTL1-WDR4 complex, blocking the m 7G modification of PKM mRNA, reducing PKM2 protein expression, disrupting the METTL1/PKM2/H3K9la positive feedback loop, and simultaneously inhibiting PKM2 nuclear translocation-mediated CD155 transcriptional activation. METTL1-WDR4-IN-1 TFA can inhibit tumor cell proliferation, weaken glycolytic metabolism, reverse tumor immune evasion (restoring NK cell and CD8 + T cell function), and regulate RNA epigenetic modification and the tumor immune microenvironment. METTL1-WDR4-IN-1 TFA can be used in immunotherapy research for cancers such as colorectal cancer, and is particularly suitable for use in combination with PKM2 inhibitors to enhance anti-tumor treatment efficacy .
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1
1 Cited Publications
Cat. No.: HY-D1056B3
Synonyms: LPS, from bacterial (Klebsiella pneumoniae)
Lipopolysaccharides, from Klebsiella pneumoniae (LPS, from bacterial (Klebsiella pneumoniae)) are lipopolysaccharide endotoxins and TLR4 activators derived from Klebsiella pneumoniae, and are classified as S-type LPS. Lipopolysaccharides, from Klebsiella pneumoniae exhibit a typical three-part structure: O-antigen, core oligosaccharide, and lipid A. Lipopolysaccharides, from Klebsiella pneumoniae may participate in bacterial immune evasion by inhibiting complement-mediated killing and suppressing the host's secretion of antimicrobial peptides, thereby allowing the bacteria to escape immune defenses. Lipopolysaccharides, from Klebsiella pneumoniae possess high viscosity and resistance to serum-mediated killing, which may lead to sepsis. Lipopolysaccharides, from Klebsiella pneumoniae can be used to construct Acute Lung Injury Model .
It is recommended to prepare a solution with concentration ≥2 mg/mL. Vortex thoroughly for more than 10 minutes. Due to the adsorption characteristics of LPS, silanized container or low adsorption centrifuge tubes should be used for aliquoting and storage, and mix thoroughly before use.
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Cat. No.: HY-D0195
CAS No.: 55589-62-3
Acesulfame potassium is a synthetic sweetener. Long-term use of Acesulfame potassium can affect cognitive function, possibly by altering the neurometabolic functions in mice. Acesulfame potassium can suppress autophagic degradation of PD-L1 in RIL-175 and SK-Hep1 cells through the ERK1/2-mTORC1-ULK1 pathway, which may be related to immune evasion in cancer cells. Acesulfame potassium can be used in research on neurological diseases, metabolic disorders, cancer, and immune evasion .
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Cat. No.: HY-176785S
MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with Kds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC50s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer .
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Cat. No.: HY-P2754
CAS No.: 9013-53-0
Target:  

Endonuclease Bacterial

Research Areas:  

Infection

Micrococcal nuclease is a secreted nuclease from Staphylococcus aureus. It digests single-stranded and double-stranded DNA (ssDNA and dsDNA) as well as RNA, cleaves oligonucleotide linkers with T-T sites, and cuts neutrophil extracellular traps and biofilm extracellular DNA into mononucleotides and dinucleotides. Micrococcal nuclease stimulates the formation of Staphylococcus aureus biofilms and mediates immune evasion. It triggers on-demand release of antibiotics from hydrogel coatings, prolongs the formation of neutrophil extracellular traps, and promotes the dissemination and survival of MRSA during infection. Micrococcal nuclease is applicable to research and characterization related to Staphylococcus aureus infection .
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Cat. No.: HY-172767
Target:  

PROTACs STAT Apoptosis

Research Areas:  

Cancer

STAT3-D11-PROTAC-VHL (Compound D11-PROTAC) is a PROTAC degrader targeting Signal Transducer and Activator of Transcription 3 (STAT3). STAT3-D11-PROTAC-VHL exhibits anti-tumor activity with IC50 values of 1335 nM and 1973 nM against HeLa and MCF-7 cells, respectively. STAT3-D11-PROTAC-VHL binds to the DNA-binding domain of STAT3 and recruits the E3 ligase VHL to form a ternary complex, leading to the ubiquitination of STAT3 and subsequent degradation by the proteasome. STAT3-D11-PROTAC-VHL also inhibits tumor cell growth, induces cell cycle arrest and apoptosis, and suppresses tumor immune evasion .
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Cat. No.: HY-161774
CAS No.: 3080717-78-5
Target:  

CD73

Research Areas:  

Cancer

ST80 is an inhibitor for interaction of OTUD4 and CD73. ST80 decreases CD73 protein level, increases CD73 protein turnover, reduces immune evasion of tumor cells, and thus exhibits antitumor efficacy against immunosuppressive triple-negative breast cancer (TNBC) .
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Cat. No.: HY-178160
CAS No.: 1581755-42-1
Target:  

SARS-CoV Virus Protease

Research Areas:  

Infection

SARS-CoV-2 PLpro-IN-2 (Compound 12) is a highly selective SARS-CoV-2 papain-like protease (PLpro) inhibitor of (IC50=0.06 μM). SARS-CoV-2 PLpro-IN-2 inhibits viral replication and immune evasion. SARS-CoV-2 PLpro-IN-2 exhibits antiviral efficacy in HeLa-ACE2 cells (EC50=2.9 μM). SARS-CoV-2 PLpro-IN-2 is promising for research of COVID-19 .
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Cat. No.: HY-176874
CAS No.: 2944114-41-2
Research Areas:  

Inflammation/Immunology Cancer

Enpp-1-IN-29 (Compound 1) is a highly selective ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) inhibitor (IC50=0.05 nM). Enpp-1-IN-29 is promising for research of ENPP1-overexpressing cancers (e.g., breast cancer, head/neck cancer, metastatic chromosome-unstable tumors) and immune-related diseases (e.g., autoimmune disorders, tumor immune evasion) .
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Cat. No.: HY-W550739
CAS No.: 33665-90-6
Acesulfame is a synthetic sweetener. Long-term use of Acesulfame can affect cognitive function. Acesulfame potassium can suppress autophagic degradation of PD-L1 in RIL-175 and SK-Hep1 cells through the ERK1/2-mTORC1-ULK1 pathway, which may be related to immune evasion in cancer cells. Acesulfame can be used in research on neurological diseases, metabolic disorders, cancer, and immune evasion .
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Cat. No.: HY-149362
Target:  

SARS-CoV

Research Areas:  

Infection

MTase-IN-1 (compound 26) is a potent and selective inhibitor of coronavirus nsp14 N7-methyltransferases, with an IC50 of 0.72 nM. MTase-IN-1 impairs viral RNA translation and immune evasion .
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Cat. No.: HY-D0195R
CAS No.: 55589-62-3
Acesulfame potassium (Standard) is the analytical standard of Acesulfame potassium (HY-D0195). This product is intended for research and analytical applications. Acesulfame potassium is a synthetic sweetener. Long-term use of Acesulfame potassium can affect cognitive function, possibly by altering the neurometabolic functions in mice. Acesulfame potassium can suppress autophagic degradation of PD-L1 in RIL-175 and SK-Hep1 cells through the ERK1/2-mTORC1-ULK1 pathway, which may be related to immune evasion in cancer cells. Acesulfame potassium can be used in research on neurological diseases, metabolic disorders, cancer, and immune evasion .
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Cat. No.: HY-174313
Antibacterial agent 284 (Compound 7) is an Antibacterial agent. Antibacterial agent 284 has a zinc-binding structure and potent inhibitory activity against Legionella pneumophila metalloprotease ProA (IC50: 0.96 μM) with zinc-binding structure. Antibacterial agent 284 significantly inactivates the cleavage of collagen IV and flagellin (ProA substrates) and reduces immune evasion from the TLR5-NF-κB pathway and PMN-mediated inflammation in human lung tissue explants. Antibacterial agent 284 is promising for Legionnaires' disease research .
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Cat. No.: HY-169262
CAS No.: 1001957-60-3
Target:  

Phospholipase Apoptosis

Research Areas:  

Cancer

PLD-IN-1 (Compound 3r) is an orally active inhibitor for phospholipase D with an IC50 of 1.97 μM. PLD-IN-1 reduces the expression of CD24, CD47 and PD-L1, enhances the calreticulin expression, and thus modulates the immune evasion mechanism in lung cancer cells by promoting the phagocytosis of cancer cells by macrophages. PLD-IN-1 inhibits the cell viability of lung cancer cell A549, HCC44, H460 and HCC15 with IC50 of 18.44, 22.31, 24.85 and 21.45 μM, respectively. PLD-IN-1 can induce apoptosis and inhibits migration in cell A549. PLD-IN-1 enhances the level of pro-inflammatory M1 macrophages and decreases the level of anti-inflammatory M2 macrophages, exhibits antitumor efficacy in mouse model .
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Cat. No.: HY-L234
83 compounds

Nucleotide metabolism is central to cancer aggressiveness, underpinning uncontrolled proliferation, chemotherapy resistance, immune evasion, and metastasis. It is transcriptionally regulated by oncogenes (e.g., MYC) and tumor suppressors (e.g., pRb). Nucleotide imbalance and nucleoside degradation further regulate cell state transitions, especially following replication stress. Additionally, secretion of nucleotides/nucleosides into the tumor microenvironment modulates immune responses and influences treatment efficacy. Therefore, nucleotide metabolites have roles in disease response and indication in cancer research, and can be utilized to develop cancer-related mechanisms and drugs.

MCE can provide 83 metabolites produced by nucleotide metabolic pathways, which can be used for disease mechanism research and drug research.

Cat. No.: HY-L250
61 compounds

In the progression of various diseases, metabolic reprogramming has emerged as a key hallmark. Lactate, as an important metabolic signaling molecule, is widely involved in tumorigenesis, immune regulation, and inflammatory responses. Particularly within the tumor microenvironment, the abnormal accumulation of lactate not only affects cellular energy metabolism but also promotes disease progression by modulating immune cell functions and mediating protein lactylation, thereby participating in epigenetic regulation and signaling networks. Therefore, systematic investigation of lactate metabolic pathways and their associated metabolites is of great significance for understanding disease mechanisms and developing novel therapeutic strategies.

The MCE lactic acid metabolite compound library contains 61 compounds and is constructed around key metabolic pathways involving lactate production, transport, and utilization. This library systematically includes core intermediates from glycolysis, the tricarboxylic acid (TCA) cycle, and the lactate cycle. Focusing on disease-associated metabolic reprogramming, it is suitable for research in oncology, inflammation, and metabolic disorders. The library can be used to elucidate the roles of lactate in tumor microenvironment regulation, immune evasion, and epigenetic modifications (such as protein lactylation). In addition, it provides high-quality small-molecule resources for drug screening, facilitating the discovery of potential modulators targeting key enzymes (such as LDH) or transporters (such as MCTs) involved in lactate metabolism.

Cat. No.: HY-L204
582 compounds

Lactic acid metabolism is one of the key metabolic pathways within living organisms. It plays a crucial role not only in cellular energy conversion but is also closely related to a variety of physiological and pathological processes. The production and clearance of lactic acid are important indicators of cellular metabolic balance, and its abnormal regulation may lead to conditions such as lactic acidosis, muscle fatigue, and hereditary metabolic diseases. Moreover, lactic acid is closely related to the malignancy of tumors and is considered a biomarker for malignant tumors and poor prognosis. Lactic acid can serve as a metabolic substrate to support the metabolic needs of tumor cells under hypoxic conditions, and it can also cause acidification of the tumor microenvironment, suppress immune cell function to promote immune evasion, and induce drug resistance in tumor cells. Currently, targeting lactic acid-lactylation and its related metabolic pathways has become a new research avenue for cancer treatment. In-depth exploration of the molecular mechanisms of lactic acid metabolism can help in screening lead compounds that regulate the lactic acid metabolism.

MCE contains 582 small molecule compounds targeting enzymes involved in lactic acid metabolism. This library is of significant value for researching the role of lactate metabolism in the mechanisms of diseases.

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