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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
79 Results for "
Gene mutation
" in MedChemExpress (MCE) Product Catalog:
Products (79)
79 Results for "Gene mutation" in MCE Product Catalog:
Cat. No.: HY-178786
CAS No.: 2491726-04-4
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RET-IN-31 (Compound 13) is an orally active, selective RET inhibitor (IC50s: 1.4 nM, 1.9 nM, 3.8 nM for RET WT, RET V804L, RET V804M, respectively). RET-IN-31 inhibits hERG and Cytochrome P450 (IC50s: 13.6 μM, 7.9 μM, 12.8 μM, 16.9 μM, 8.9 μM, 13.0 μM for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4-M, CYP3A4-T, respectively). RET-IN-31 has anti-cancer effects against activated RET mutations and gene fusion-driven cancers .
Cat. No.: HY-P5369
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Cat. No.: HY-P5365
CAS No.: 374796-72-2
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Metazide is an antitubercular agent with non-mutagenic properties. Metazide does not induce gene mutations in Salmonella typhimurium tester strains TA 1950 and TA 1538 with in vitro metabolic activation via modified Ames plate technique. Metazide can be used for the research of tuberculosis .
Cat. No.: HY-101977A
CAS No.: 2097002-59-8
Synonyms: (R,S)-LOXO-195
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(R,S)-Selitrectinib ((R,S)-LOXO-195) (compound 17) is a Trk inhibitor with activity against cancers harboring Trk inhibitor-resistant point mutations in NTRK1, NTRK2, or NTRK3 genes. (R,S)-Selitrectinib can be used for the research of trk inhibitor-resistant cancer .
Cat. No.: HY-P2858H
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β-Mannosidase, Streptomyces coelicolor (EC 3.2.1.25) catalyses the following chemical reaction:Hydrolysis of terminal, non-reducing beta-D-mannose residues in beta-D-mannosides. This gene encodes a member of the glycosyl hydrolase 2 family. The encoded protein localizes to the lysosome where it is the final exoglycosidase in the pathway for N-linked glycoprotein oligosaccharide catabolism. Mutations in this gene are associated with beta-mannosidosis, a lysosomal storage disease that has a wide spectrum of neurological involvement.
Cat. No.: HY-E70894
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α,γ-Homocysteinase, Trichomonas vaginalis is a pyridoxal-5’-phosphate dependent enzyme. α,γ-Homocysteinase, Trichomonas vaginalis is a mutant of homocysteinase from Trichomonas vaginalis encoded by mgl1 gene, containing three point mutations, such as; Phe47Leu, Asp172Glu, Ser308Tyr. α,γ-Homocysteinase, Trichomonas vaginalis can metabolize homocysteine into α-keto butyrate, hydrogen sulfide and ammonia.
Cat. No.: HY-L015
1,149 compounds
The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials.
MCE owns a unique collection of 1,149 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.
Fenaminosulf is a plant immune modulator and mutagen. Fenaminosulf impairs plant immune recognition and signal transduction by inhibiting the activities of key kinases such as Xa21 and PBL19, thereby regulating the expression of genes related to hormone metabolism, phenylpropane biosynthesis, and plant-pathogen interactions. Fenaminosulf affects the growth and gall formation of Zizania latifolia in a concentration-dependent manner. Fenaminosulf induces mutations in bacterial systems and causes plant chromosome aberrations, but shows no mutagenic activity or lethal effect in Drosophila melanogaster. Fenaminosulf exhibits inconsistent carcinogenicity in rat studies .
Cat. No.: HY-147412D
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FAM labled Ultevursen sodiumis a FAM labled Ultevursen sodium (HY-147412A). Ultevursen sodium (QR-421a) is a splice-modulating antisense oligonucleotide targeting exon 13 of the USH2A gene, which restores the functional expression of Usherin protein by inducing exon skipping. Ultevursen sodium binds to USH2A pre-mRNA and modulates the splicing process to specifically skip exon 13 carrying the pathogenic mutation c.2299delG, generating an in-frame transcript and a truncated yet functionally normal protein. Ultevursen sodium exhibits concentration-dependent exon skipping activity in human cells and retinal organoid models, and restores Usherin expression and retinal function in zebrafish and gene-edited mouse models. Ultevursen sodium can be used for related research on type 2 Usher syndrome and non-syndromic retinitis pigmentosa .
Cat. No.: HY-147412E
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Cy3 labled Ultevursen sodium is a Cy3 labled Ultevursen sodium (HY-147412A). Ultevursen sodium (QR-421a) is a splice-modulating antisense oligonucleotide targeting exon 13 of the USH2A gene, which restores the functional expression of Usherin protein by inducing exon skipping. Ultevursen sodium binds to USH2A pre-mRNA and modulates the splicing process to specifically skip exon 13 carrying the pathogenic mutation c.2299delG, generating an in-frame transcript and a truncated yet functionally normal protein. Ultevursen sodium exhibits concentration-dependent exon skipping activity in human cells and retinal organoid models, and restores Usherin expression and retinal function in zebrafish and gene-edited mouse models. Ultevursen sodium can be used for related research on type 2 Usher syndrome and non-syndromic retinitis pigmentosa .
Cat. No.: HY-187090
CAS No.: 69658-91-9
Synonyms: 3-NMPY
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3-N-Nitroso-N-methylaminopyridine is a non-carcinogenic, non-mutagenic arylalkyl nitrosamine isomer that serves as a substrate for enzymatic metabolic processes. 3-N-Nitroso-N-methylaminopyridine undergoes enzymatic denitrosation, enzymatic N-oxide formation, and limited oxidative demethylation to produce trace amounts of 3-hydroxypyridine. 3-N-Nitroso-N-methylaminopyridine directly induces gene mutations in E. coli, but its mutagenic potential is eliminated by the rodent liver S-100 fraction. 3-N-Nitroso-N-methylaminopyridine shows no carcinogenicity in rats and no mutagenicity in the Ames test . 3-NMPY can be used in studies related to the metabolism and carcinogenic mechanisms of nitrosamine compounds in vitro and in vivo .
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Dihydralazine sulfate (Standard) is the analytical standard of Dihydralazine sulfate (HY-N7065). This product is intended for research and analytical applications. Dihydralazine sulfate is an antihypertensive hydrazine derivative and also a low-potency genotoxic agent. Dihydralazine sulfate is a direct-acting mutagen with a mixed gene mutation mechanism, which induces DNA fragmentation in the lung, kidney and spleen of mice, and induces sister chromatid exchange in mouse bone marrow cells. Dihydralazine sulfate specifically kills DNA repair-deficient bacteria. Dihydralazine sulfate is a vasodilator and antihypertensive agent that reduces systemic vascular resistance, increases cardiac output and heart rate, thereby lowering blood pressure. Dihydralazine sulfate can be used in research related to hypertension and severe early-onset preeclampsia .
Cat. No.: HY-156794A
Synonyms: DSP-5336 enantiomer
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Enzomenib enantiomer (DSP-5336 enantiomer) is an enantiomer of Enzomenib (HY-156794). Enzomenib (DSP-5336) is an orally active Menin inhibitor (IC50=1.4 nM, Kd=6.0 nM). Enzomenib disrupts the interaction between Menin and KMT2A/MLL fusion proteins, specifically inhibits the expression of leukemia driver genes such as HOX/MEIS1, and upregulates ITGAM. Enzomenib effectively induces cell differentiation, inhibits tumor cell proliferation, and suppresses primitive cell colony formation. Enzomenib reduces disease burden and prolongs survival, but causes adverse reactions including differentiation syndrome and QTc interval prolongation. Enzomenib is used for research on relapsed/refractory acute myeloid leukemia, acute lymphoblastic leukemia, and other hematologic malignancies with mixed lineage leukemia (MLL) rearrangements or NPM1 mutations .
Cat. No.: HY-L004
3,522 compounds
DNA is prone to numerous forms of damage that can injure cells and impair fitness. Cells have developed an array of mechanisms to repair these injuries. Proliferating cells are especially vulnerable to DNA damage due to the added demands of cellular growth and division. Cell cycle checkpoints represent integral components of DNA repair that coordinate cooperation between the machinery of the cell cycle and several biochemical pathways that respond to damage and restore DNA structure. By delaying progression through the cell cycle, checkpoints provide more time for repair before the critical phases of DNA replication, when the genome is replicated, and of mitosis, when the genome is segregated. Loss or attenuation of checkpoint function may increase spontaneous and induced gene mutations and chromosomal aberrations by reducing the efficiency of DNA repair.
MCE owns a unique collection of 3,522 cell cycle/DNA damage-related compounds which can be used in the research of the same.
Cat. No.: HY-L011
2,278 compounds
Most of molecules enter or leave cells mainly via membrane transport proteins, which play important roles in several cellular functions, including cell metabolism, ion homeostasis, signal transduction, the recognition process in the immune system, energy transduction, etc. There are three major types of transport proteins, ATP-powered pumps, channel proteins and transporters. Transport proteins such as channels and transporters play important roles in the maintenance of intracellular homeostasis, and mutations in these transport protein genes have been identified in the pathogenesis of a number of hereditary diseases. In the central nervous system, ion channels have been linked to, but not limited to, many diseases such asataxias, paralyses, epilepsies, and deafness. This indicates the roles of ion channels in the initiation and coordination of movement, sensory perception, and encoding and processing of information. Ion channels are a major class of drug targets in drug development.
MCE designs a unique collection of 2,278 smal-molecule modulators that can be used for the research of Ion Channel and Membrane Transporter or high throughput screening (HTS) related drug discovery.
Cat. No.: HY-L101
3,003 compounds
Liver cancer is one of the leading malignancies which occupies the second position in cancer deaths worldwide, becoming serious threat to human health. Hepatocellular carcinoma (HCC), also known as hepatoma is the most common type accounting for approximately 90% of all liver cancers.
Current evidence indicates that during hepatocarcinogenesis, two main pathogenic mechanisms prevail: (1) cirrhosis associated with hepatic regeneration after tissue damage caused by hepatitis infection, toxins or metabolic influences, and (2) mutations occurring in single or multiple oncogenes or tumor suppressor genes. Both mechanisms have been linked with alterations in several important cellular signaling pathways. These include the RAF/MEK/ERK pathway, PI3K/AKT/mTOR pathway, WNT/b-catenin pathway, insulin-like growth factor pathway, c-MET/HGFR pathway , etc.
MCE offers a unique collection of 3,003 compounds with identified and potential anti-liver cancer activity. MCE anti-liver cancer compound library is a useful tool for anti-liver cancer drugs screening and other related research.
Cat. No.: HY-L260
82 compounds
KRAS (Kirsten Rat Sarcoma Viral Oncogene Homolog) is one of the most important oncogenic driver genes in oncology, with high mutation frequencies in pancreatic cancer, non‑small cell lung cancer, and colorectal cancer. For a long time, KRAS was considered "undruggable" due to the lack of suitable small‑molecule binding pockets on its protein surface. In recent years, with the discovery of the switch‑II pocket and the successful approval of KRAS G12C inhibitors, KRAS‑targeted research has achieved groundbreaking progress, which has also spurred a wave of development targeting non‑G12C mutants such as G12D and G12V, as well as upstream and downstream regulatory factors including SOS1 and SHP2.
MCE KRAS Targeted Compound Library contains 82 small‑molecule compounds targeting the KRAS, serving as high‑quality research tools for mechanistic studies of KRAS‑mutant tumors, combination therapy development, resistance mechanism exploration, and high‑throughput drug screening, thereby providing robust support for KRAS‑targeted drug discovery.
Cat. No.: HY-L083
3,806 compounds
Mutations in oncogenes and tumor suppressor genes can modify multiple signaling pathways and in turn cell metabolism, which facilitates tumorigenesis. The paramount hallmark of tumor metabolism is “aerobic glycolysis” or the Warburg effect, coined by Otto Warburg in 1926, in which cancer cells produce most of energy from glycolysis pathway regardless of whether in aerobic or anaerobic condition. Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside. The increased uptake of glucose is facilitated by the overexpression of several isoforms of membrane glucose transporters (GLUTs). Likewise, the metabolic pathways of glutamine, amino acid and fat metabolism are also altered. Recent trends in anti-cancer drug discovery suggests that targeting the altered metabolic pathways of cancer cells result in energy crisis inside the cancer cells and can selectively inhibit cancer cell proliferation by delaying or suppressing tumor growth.
MCE provides a unique collection of 3,806 compounds which cover various tumor metabolism-related signaling pathways. These compounds can be used for anti-cancer metabolism targets identification, validation as well anti-cancer drug discovery.
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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
