目录号 | 产品详情 | 靶点 | |
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T33659 | |||
Nicardipine pyridine metabolite II is a biaoctive chemical. | |||
T11641 | Bcr-Abl PDGFR c-Kit Drug Metabolite | ||
N-Desmethyl imatinib (Imatinib metabolite N-Desmethyl imatinib) 是 Imatinib 的代谢物。Imatinib 是一个靶向 c-Kit、v-Abl 和 PDGFR 的多靶点抑制剂。 | |||
T71932 | |||
MAM2201 N-pentanoic acid metabolite is a potential phase 1 metabolite of MAM2201 -- a cannabinoid receptor agonist. | |||
T13525 | Others | ||
Abiraterone metabolite 1 is a 5β-reduced metabolite of abiraterone. Abiraterone inhibits CYP17A1, blocks androgen synthesis, and prolongs survival in prostate cancer. | |||
T19406 | Others | ||
Lurasidone Metabolite 14283 D8 is the deuterium labeled Lurasidone Metabolite 14283. | |||
T19407 | Others | ||
Lurasidone Metabolite 14326 D8 is the deuterium labeled Lurasidone Metabolite 14326. | |||
T13760 | Others | ||
Lurasidone Metabolite 14283 hydrochloride is a major active metabolite of Lurasidone. | |||
T12212 | Others | ||
N-desmethyl Netupitant is a highly selective antagonist of NK1 receptor, and is Netupitant metabolite. | |||
T11637 | Others | ||
Iloperidone metabolite Hydroxy Iloperidone is an atypical antipsychotic. It is a metabolite of Iloperidone. | |||
T12211 | Others | ||
Monohydroxy Netupitant is a highly selective antagonist of NK1 receptor, and is Netupitant metabolite. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-00844 | HSD11B2 Protein, Human, Recombinant (His) | Human | Yeast | ||
Catalyzes the conversion of cortisol to the inactive metabolite cortisone. Modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids.
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TMPH-00843 | HSD11B1 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Catalyzes reversibly the conversion of cortisol to the inactive metabolite cortisone. Catalyzes reversibly the conversion of 7-ketocholesterol to 7-beta-hydroxycholesterol. In intact cells, the reaction runs only in one direction, from 7-ketocholesterol to 7-beta-hydroxycholesterol.
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TMPY-03414 | ABHD10 Protein, Human, Recombinant (aa 53-306, His) | Human | Baculovirus-Insect Cells | ||
Mycophenolic acid (MPA), the active metabolite of the immunosuppressant mycophenolate mofetil (MMF), is primarily metabolized by glucuronidation to a phenolic glucuronide (MPAG) and an acyl glucuronide (AcMPAG). It is known that AcMPAG, which may be an immunotoxic metabolite, is deglucuronidated in human liver. AcMPAG deglucuronidation activity was detected in both human liver cytosol (HLC) and microsomes (HLM). By purification from HLC with column chromatographic purification steps, the enzyme responsible for AcMPAG deglucuronidationis identified as α/β hydrolase domain containing 1 (ABHD1). Recombinant ABHD1 expressed in Sf9 cells efficiently deglucuronidated AcMPAG with a K(m) value of 1.7 ± 1.2 μM, which was similar to those in HLM, HLC, and human liver homogenates (HLH). Immunoblot analysis revealed ABHD1 protein expression in both HLC and HLM. The AcMPAG deglucuronidation by recombinant ABHD1, HLC, and HLH were potently inhibited by AgNO(3), CdCl(2), CuCl(2), PMSF, bis-p-nitrophenylphosphate, and DTNB. The CL(int) value of AcMPAG formation from MPA, which was catalyzed by human UGT2B7, in HLH was increased by 1.8-fold in the presence of PMSF. Thus, human ABHD1 would affect the formation of AcMPAG, the immunotoxic metabolite.
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TMPY-00320 | APOA1BP Protein, Human, Recombinant (His) | Human | HEK293 | ||
APOA1BP, now renamed NAXE, encodes an epimerase essential in the cellular metabolite repair for NADHX and NADPHX. The enzyme catalyzes the epimerization of NAD(P)HX, thereby avoiding the accumulation of toxic metabolites.Pathogenic biallelic mutations in NAXE in children from four families with (sub-) acute-onset ataxia, cerebellar edema, spinal myelopathy, and skin lesions.
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TMPH-02615 | CBS Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Hydro-lyase catalyzing the first step of the transsulfuration pathway, where the hydroxyl group of L-serine is displaced by L-homocysteine in a beta-replacement reaction to form L-cystathionine, the precursor of L-cysteine. This catabolic route allows the elimination of L-methionine and the toxic metabolite L-homocysteine. Also involved in the production of hydrogen sulfide, a gasotransmitter with signaling and cytoprotective effects on neurons.
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TMPH-01597 | KYAT1 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Catalyzes the irreversible transamination of the L-tryptophan metabolite L-kynurenine to form kynurenic acid (KA), an intermediate in the tryptophan catabolic pathway which is also a broad spectrum antagonist of the three ionotropic excitatory amino acid receptors among others. Also metabolizes the cysteine conjugates of certain halogenated alkenes and alkanes to form reactive metabolites. Catalyzes the beta-elimination of S-conjugates and Se-conjugates of L-(seleno)cysteine, resulting in the cleavage of the C-S or C-Se bond.
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TMPH-02469 | PDK1 Protein, Mouse, Recombinant (His) | Mouse | Baculovirus | ||
Kinase that plays a key role in regulation of glucose and fatty acid metabolism and homeostasis via phosphorylation of the pyruvate dehydrogenase subunits PDHA1 and PDHA2. This inhibits pyruvate dehydrogenase activity, and thereby regulates metabolite flux through the tricarboxylic acid cycle, down-regulates aerobic respiration and inhibits the formation of acetyl-coenzyme A from pyruvate. Plays an important role in cellular responses to hypoxia and is important for cell proliferation under hypoxia. Protects cells against apoptosis in response to hypoxia and oxidative stress.
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TMPY-02420 | HEMK2 Protein, Human, Recombinant (His) | Human | E. coli | ||
N6AMT1 (N-6 Adenine-Specific DNA Methyltransferase 1) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. This gene encodes an N(6)-adenine-specific DNA methyltransferase. It belongs to the eukaryotic/archaeal PrmC-related family. The encoded enzyme may be involved in the methylation of release factor I during translation termination. N6AMT1 has a significant role in determining susceptibility to arsenic toxicity and carcinogenicity because of its specific activity in methylating MMAIII to DMA and other unknown mechanisms. N6AMT1 methylates the toxic inorganic arsenic (iAs) metabolite, monomethylarsonous acid (MMA), to the less toxic dimethylarsinic acid (DMA). N6AMT1 polymorphisms were associated with arsenic methylation in Andean women, independent of AS3MT.
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TMPH-01598 | CCBL2 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Catalyzes the irreversible transamination of the L-tryptophan metabolite L-kynurenine to form kynurenic acid (KA), an intermediate in the tryptophan catabolic pathway which is also a broad spectrum antagonist of the three ionotropic excitatory amino acid receptors among others. May catalyze the beta-elimination of S-conjugates and Se-conjugates of L-(seleno)cysteine, resulting in the cleavage of the C-S or C-Se bond. Has transaminase activity towards L-kynurenine, tryptophan, phenylalanine, serine, cysteine, methionine, histidine, glutamine and asparagine with glyoxylate as an amino group acceptor (in vitro). Has lower activity with 2-oxoglutarate as amino group acceptor (in vitro).
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TMPH-02877 | RIPK3 Protein, Mouse, Recombinant (His) | Mouse | Yeast | ||
Serine/threonine-protein kinase that activates necroptosis and apoptosis, two parallel forms of cell death. Necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members, is triggered by RIPK3 following activation by ZBP1. Activated RIPK3 forms a necrosis-inducing complex and mediates phosphorylation of MLKL, promoting MLKL localization to the plasma membrane and execution of programmed necrosis characterized by calcium influx and plasma membrane damage. In addition to TNF-induced necroptosis, necroptosis can also take place in the nucleus in response to orthomyxoviruses infection: following ZBP1 activation, which senses double-stranded Z-RNA structures, nuclear RIPK3 catalyzes phosphorylation and activation of MLKL, promoting disruption of the nuclear envelope and leakage of cellular DNA into the cytosol. Also regulates apoptosis: apoptosis depends on RIPK1, FADD and CASP8, and is independent of MLKL and RIPK3 kinase activity. Phosphorylates RIPK1: RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation. In some cell types, also able to restrict viral replication by promoting cell death-independent responses. In response to flavivirus infection in neurons, promotes a cell death-independent pathway that restricts viral replication: together with ZBP1, promotes a death-independent transcriptional program that modifies the cellular metabolism via up-regulation expression of the enzyme ACOD1/IRG1 and production of the metabolite itaconate. Itaconate inhibits the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes. RIPK3 binds to and enhances the activity of three metabolic enzymes: GLUL, GLUD1, and PYGL. These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production.
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TMPH-00839 | RIPK3 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Serine/threonine-protein kinase that activates necroptosis and apoptosis, two parallel forms of cell death. Necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members, is triggered by RIPK3 following activation by ZBP1. Activated RIPK3 forms a necrosis-inducing complex and mediates phosphorylation of MLKL, promoting MLKL localization to the plasma membrane and execution of programmed necrosis characterized by calcium influx and plasma membrane damage. In addition to TNF-induced necroptosis, necroptosis can also take place in the nucleus in response to orthomyxoviruses infection: following ZBP1 activation, which senses double-stranded Z-RNA structures, nuclear RIPK3 catalyzes phosphorylation and activation of MLKL, promoting disruption of the nuclear envelope and leakage of cellular DNA into the cytosol. Also regulates apoptosis: apoptosis depends on RIPK1, FADD and CASP8, and is independent of MLKL and RIPK3 kinase activity. Phosphorylates RIPK1: RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation. In some cell types, also able to restrict viral replication by promoting cell death-independent responses. In response to Zika virus infection in neurons, promotes a cell death-independent pathway that restricts viral replication: together with ZBP1, promotes a death-independent transcriptional program that modifies the cellular metabolism via up-regulation expression of the enzyme ACOD1/IRG1 and production of the metabolite itaconate. Itaconate inhibits the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes. RIPK3 binds to and enhances the activity of three metabolic enzymes: GLUL, GLUD1, and PYGL. These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production.; (Microbial infection) In case of herpes simplex virus 1/HHV-1 infection, forms heteromeric amyloid structures with HHV-1 protein RIR1/ICP6 which may inhibit RIPK3-mediated necroptosis, thereby preventing host cell death pathway and allowing viral evasion.
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