EC Number   |
Recommended Name |
Application |
|---|
    1.1.1.1 | alcohol dehydrogenase |
pharmacology |
the alcohol dehydrogenase effectively catalyzes the reductions of various substituted alpha-chloroacetophenones to form the (R)-enantiomer of the corresponding chlorohydrins with excellent ennatiomeric purity. The co-factor NADH can be recycled by the D-glucose dehydrogenase and D-glucose regeneration system or via the simple hydrogen transfer mode using iso-propanol as the hydrogen donor. The applicability of the alcohol-dehydrogenase-catalyzed hydrogen transfer reduction in the synthesis of optically active chlorohydrins is demonstrated by carrying out several reductions on the preparative scale. Thus enzyme is a valuable biocatalyst for the preparation of chiral chlorohydrins of pharmaceutical interest |
| 1.1.1.3 | homoserine dehydrogenase |
pharmacology |
enzyme is a target for inhibitor design for construction of antimicrobial agents |
| 1.1.1.10 | L-xylulose reductase |
pharmacology |
enzyme is a target for design and development of potent and specific structure-based inhibitors binding in the active site |
| 1.1.1.17 | mannitol-1-phosphate 5-dehydrogenase |
pharmacology |
inhibition of AfM1PDH might be a useful target for therapy of Aspergillus fumigatus infections |
| 1.1.1.B18 | L-1-amino-2-propanol dehydrogenase |
pharmacology |
the enzyme produces double chiral aminoalcohols, which are used as pharmaceuticals. The Rhodococcus expression vector, pRET11100, constructed by removing aadh from the pRET1172 plasmid may be useful for bioconversion |
| 1.1.1.22 | UDP-glucose 6-dehydrogenase |
pharmacology |
target for inhibitor design |
| 1.1.1.35 | 3-hydroxyacyl-CoA dehydrogenase |
pharmacology |
the short-chain 3-hydroxyacyl-CoA dehydrogenase is a target for intervention in case of Alzheimer's disease and Parkinson's disease |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
pharmacology |
the enzyme is an important therapeutic target for diabetes in humans |
| 1.1.1.44 | phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating) |
pharmacology |
the enzyme is a target for inhibitor development for usage as drugs against African Trypanosomiasis |
| 1.1.1.B51 | 3-quinuclidinone reductase (NADPH) |
pharmacology |
stereospecific production of (R)-3-quinuclidinol, an important chiral building block for the synthesis of various pharmaceuticals |
| 1.1.1.B52 | 3-quinuclidinone reductase (NADH) |
pharmacology |
stereospecific production of (R)-3-quinuclidinol, an important chiral building block for the synthesis of various pharmaceuticals |
| 1.1.1.B52 | 3-quinuclidinone reductase (NADH) |
pharmacology |
stereospecific production of (R)-3-quinuclidinol, an important chiral building block for the synthesis of various pharmaceuticals, high yield of (R)-3-quinuclidinol up to 916 g/L * d using a bioreduction approach |
| 1.1.1.B52 | 3-quinuclidinone reductase (NADH) |
pharmacology |
stereospecific production of (R)-3-quinuclidinol, an important chiral building block for the synthesis of various pharmaceuticals. The 3-quinuclidinone reductase and Leifsonia sp. alcohol dehydrogenase genes are efficiently expressed in Escherichia coli cells. A number of constructed Echerichia coli biocatalysts (intact or immobilized) are applied to the resting cell reaction and optimized. Under the optimized conditions, (R)-(-)-3-quinuclidinolis synthesized from 3-quinuclidinone (15% w/v, 939 mM) giving a conversion yield of 100% for the immobilized enzyme. The optical purity of the (R)-(-)-3-quinuclidinol produced by the enzymatic reactions is above 99.9% |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
pharmacology |
isozyme 11beta-HSD1 is a target in treatment of metabolic diseases such as diabetes mellitus type 2 or obesity |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
pharmacology |
the enzyme is an important therapeutic target for diabetes in humans |
| 1.1.1.188 | prostaglandin-F synthase |
pharmacology |
enzyme is a target for cyclooxygenase-independent antineoplastic actions of nonsteroidal anti-inflammatory drugs |
| 1.1.1.205 | IMP dehydrogenase |
pharmacology |
the enzyme is a potential target as modulators in MTX chemotherapy of resistant cells, overview |
| 1.1.1.282 | quinate/shikimate dehydrogenase [NAD(P)+] |
pharmacology |
enzymes of the shikimate pathway has been promoted as a target for the development of antimicrobial agents |
| 1.1.1.300 | NADP-retinol dehydrogenase |
pharmacology |
enzyme RDH8 is a therapeutic target for controlling bis-retinoid A2E cytotoxicity |
| 1.1.1.326 | zerumbone synthase |
pharmacology |
zerumbone is a predominating potential multi-anticancer agent |
| 1.1.99.21 | D-sorbitol dehydrogenase (acceptor) |
pharmacology |
miglitol (N-hydroxyethyl-1-deoxynojirimycin), a type of hypoglycemic drug works by competitively inhibiting alpha-glucosidase activity to control postprandial blood glucose, can be used in the treatment of type II diabetes mellitus. 6-(N-hydroxyethyl)-amino-6-deoxy-alpha-L-sorbofuranose, is a key intermediate for the synthesis of miglitol, is produced from N-2-hydroxyethyl glucamine (NHEG) by biotransformation with resting cells of Gluconobacter oxydans. Balanced co-expression of both the mSLDH and the PQQ synthases is effective for the industrial production of 6-(N-hydroxyethyl)-amino-6-deoxy-L-sorbofuranose |
| 1.1.99.21 | D-sorbitol dehydrogenase (acceptor) |
pharmacology |
synergistic improvement of PQQ-dependent D-sorbitol dehydrogenase activity from Gluconobacter oxydans for the biosynthesis of miglitol precursor 6-(N-hydroxyethyl)-amino-6-deoxy-alpha-L-sorbofuranose. Miglitol (N-hydroxyethyl-1-deoxynojirimycin) is a pseudomonosaccharide glucosidase inhibitor in the treatment of non-insulin-dependent mellitus |
| 1.2.1.11 | aspartate-semialdehyde dehydrogenase |
pharmacology |
enzyme is a target for development of antibiotics |
| 1.2.1.11 | aspartate-semialdehyde dehydrogenase |
pharmacology |
inhibitor design from enzyme three-dimensional structure |
| 1.2.1.12 | glyceraldehyde-3-phosphate dehydrogenase (phosphorylating) |
pharmacology |
lung-stage schistosomula immunofluorescence reactivity is diminished following antiserum absorption with reconbinant glyceraldehyde 3-phosphate dehydrogenase. Discussion of glyceraldehyde 3-phosphate dehydrogenase as a candidate vaccine antigen |
| 1.2.3.1 | aldehyde oxidase |
pharmacology |
metabolic inactivation of neonicotinoid insecticide substrates by enzyme system coupled with Drosophila nicotinic acetylcholine receptor |
| 1.3.1.9 | enoyl-[acyl-carrier-protein] reductase (NADH) |
pharmacology |
the enzyme is a target for developing novel anti-tubercular agents |
| 1.3.1.9 | enoyl-[acyl-carrier-protein] reductase (NADH) |
pharmacology |
the enzyme is a target for the antitubercular drug isoniazid. InhA inhibitors targeted at the enoyl substrate binding site may be effective against existing isoniazid-resistant strains of Mycobacterium tuberculosis |
| 1.3.1.14 | dihydroorotate dehydrogenase (NAD+) |
pharmacology |
drug design based upon selective enzyme inhibition |
| 1.3.1.22 | 3-oxo-5alpha-steroid 4-dehydrogenase (NADP+) |
pharmacology |
enzyme is a target for drug developement |
| 1.3.1.24 | biliverdin reductase |
pharmacology |
critical role for biliverdin reductase A in protecting against lipid accumulation and oxidative stress in hepatocytes which may serve as a future therapeutic target for non-alcoholic fatty liver disease (NAFLD) and its progression to non-alcoholic steatohepatitis (NASH) |
| 1.3.1.24 | biliverdin reductase |
pharmacology |
transduced fusion protein Tat-biliverdin reductase A (Tat-BLVRA) markedly inhibits cell death, DNA fragmentation, and generation of ROS. Transduced Tat-BLVRA inhibits the apoptosis and mitogen activated protein kinase (MAPK) signaling pathway and it passes through the blood-brain barrier (BBB) and significantly prevents hippocampal cell death in an ischemic model. Tat-BLVRA provides a possibility as a therapeutic molecule for ischemia |
| 1.3.1.70 | DELTA14-sterol reductase |
pharmacology |
enzyme is a potential antifungal target site, development of antifungal compounds |
| 1.3.1.72 | DELTA24-sterol reductase |
pharmacology |
3beta-hydroxysterol DELTA24-reductase on the surface of hepatitis C virus-related hepatocellular carcinoma cells can be a target for molecular targeting therapy |
| 1.3.1.118 | meromycolic acid enoyl-[acyl-carrier-protein] reductase |
pharmacology |
structural investigations of reactive isoniazid species in order to promote the design of new inhibitors of InhA as potential antituberculous drugs |
| 1.3.1.118 | meromycolic acid enoyl-[acyl-carrier-protein] reductase |
pharmacology |
the enzyme is a target for developing novel anti-tubercular agents |
| 1.3.1.118 | meromycolic acid enoyl-[acyl-carrier-protein] reductase |
pharmacology |
the enzyme is a target for the development of new anti-tubercular drugs |
| 1.3.3.12 | L-galactonolactone oxidase |
pharmacology |
because humans lack the capacity to synthesize ascorbate, the trypanosomal enzymes involved in ascorbate biosynthesis are interesting targets for drug therapy |
| 1.3.5.2 | dihydroorotate dehydrogenase (quinone) |
pharmacology |
A77 1726 inhibits cell growth in multiple myeloma cell lines at clinically achievable concentrations by induction of apoptosis. Inhibition of cell growth is partly due to inhibition of multiple myeloma cell proliferation. A77 1726 shows synergistic and additive activity together with genotoxic agents melphalan, treosulfan, and doxorubicin |
| 1.3.8.6 | glutaryl-CoA dehydrogenase (ETF) |
pharmacology |
targeted suppression of GCDH by lentivirus-mediated shRNA and excessive intake of lysine may be a useful cell model of glutaric aciduria type 1, overview |
| 1.3.98.3 | coproporphyrinogen dehydrogenase |
pharmacology |
the structure of HemN sets the stage for the development of inhibitors with antibacterial function due to the uniquely bacterial occurence of the enzyme |
| 1.3.99.38 | menaquinone-9 beta-reductase |
pharmacology |
menaquinone synthesis may be a drug target in Mycobacteria |
| 1.3.99.38 | menaquinone-9 beta-reductase |
pharmacology |
menaquinone synthesis may be a drug target in Mycobacterium tuberculosis |
| 1.4.3.3 | D-amino-acid oxidase |
pharmacology |
co-administration of the enzyme inhibitor 5-chloro-benzo[d]isoxazol-3-ol significantly enhances the efficacy of D-serine in attenuating prepulse inhibition deficits by administration of dizocilpine, an NMDA receptor antagonist. Therefore, co-administration of D-serine and a DAAO inhibitor has therapeutic potential for the treatment of schizophrenia |
| 1.4.3.3 | D-amino-acid oxidase |
pharmacology |
diminished DAO activity and elevations in D-serine may serve as an effective therapeutic intervention for the treatment of psychiatric symptoms |
| 1.4.3.14 | L-lysine oxidase |
pharmacology |
promising enzyme for further investigation as a potential anticancer agent. Antitumor effect against murine tumors and human cancer xenografts |
| 1.4.3.22 | diamine oxidase |
pharmacology |
formulation of vegetal diamine oxidase as a food supplement for the prevention of food allergy and treatment of enteric dysfunction. Study on the stability of diamine oxidase, purified from Lathyrus sativus seedlings, in various simulated intestinal media is reported. The catalytic activity of different diamine oxidase concentrations is tested in simulated intestinal media with different pH and containing cholic acids, pancreatic bicarbonate, and proteases or exogenous food- and drink-derived items, such as lipids or alcohol, alone or in combination |
| 1.4.3.22 | diamine oxidase |
pharmacology |
improved food supplements must be developed to help histamine intolerant humans. At least 50 nkat free porcine diamine oxidase are required to convert 75 mg histamine to (imidazol-4-yl)acetaldehyde in an in vitro test system. This results in a reduction of histamine by 90%. The enzyme showes weak stability under simulated intestinal conditions with a half-life period of around 19 min. Therefore, a lot more exogenous diamine oxidase would be required for efficient histamine degradation in the human intestine |
| 1.5.1.33 | pteridine reductase |
pharmacology |
successful antifolate chemotherapy in Leishmania will have to target simultaneously both pterine reductase 1 and dihydrofolate reductase-thymidylate synthase |
| 1.5.3.13 | N1-acetylpolyamine oxidase |
pharmacology |
N,N'-butanedienyl butanediamine, i.e. MDL 72527 or CPC-200, a small molecule specific inhibitor of polyamine oxidase, effectively blocks androgen-induced reactive oxygen species production in human prostate cancer cells, as well as significantly delays prostate cancer progression and death in animals developing spontaneous prostate cancer |
| 1.6.5.2 | NAD(P)H dehydrogenase (quinone) |
pharmacology |
a series of lavendamycin analogues are tested in docking studies employing an X-ray derived NQO1 active site computational model, structure-based analogue design criteria are valid, resulting in the design of two analogues with high substrate specificity and selective toxicity toward NQO1-rich cells |
| 1.7.1.B2 | aromatic nitroreductase [NAD(P)H] |
pharmacology |
Pseudomonas aeruginosa NfsB and nitro-CBI-DEI is a promising enzyme/prodrug combination for gene directed enzyme prodrug therapy |
| 1.7.3.3 | factor-independent urate hydroxylase |
pharmacology |
urate oxidase is a potential therapeutic protein in the prevention and treatment of tumor lysis syndrome and hyperuricemia. However, its severe immunogenicity limits its clinical application. Engineering site-specific modifications of keto groups in urate oxidase by using evolved Methanocaldococcus jannaschii aminoacyl-tRNA synthetase(s)/suppressor tRNA pairs reduces its antigenicity. The mutated uricase exhibits decreased antigenic properties, while its catalytic activities remain unchanged |
| 1.8.1.7 | glutathione-disulfide reductase |
pharmacology |
enzyme is a target for enzyme inhibitor and antimalarial drug development |
| 1.8.1.10 | CoA-glutathione reductase |
pharmacology |
anti-staphylococcal agent, possible target for the design of selective inhibitors that would interrupt the thiol metabolism of the human pathogen Staphylococcus aureus |
| 1.8.1.12 | trypanothione-disulfide reductase |
pharmacology |
enzyme is a drug target |
| 1.8.1.12 | trypanothione-disulfide reductase |
pharmacology |
enzyme is a target for selective drug design |
| 1.8.1.12 | trypanothione-disulfide reductase |
pharmacology |
trypanothione reductase plays a central role in the trypanosomatid parasites defense against oxidative stress, trypanothione reductase is a promising target for antitrypanosomal drugs, 2-iminobenzimidazole class are potent trypanothione reductase inhibitors against Trypanosoma brucei rhodesiense and low cytotoxicity against human cells |
| 1.8.1.12 | trypanothione-disulfide reductase |
pharmacology |
trypanothione reductase plays a central role in the trypanosomatid parasites defense against oxidative stress, trypanothione reductase is a promising target for antitrypanosomal drugs, binding affinity towards trypanothione reductase and glutathione reductase of nitrofuran derivatives is assessed by standard molecular docking procedures and both, energy and structural output analysis, nitrofuran ligands display a slight preference to bind the closely related human glutathione reductase, they should not be considered as drugs with selective inhibition of trypanothione reductase |
| 1.8.1.12 | trypanothione-disulfide reductase |
pharmacology |
trypanothione reductase plays a central role in the trypanosomatid parasites defense against oxidative stress, trypanothione reductase is a promising target for antitrypanosomal drugs, novel inhibitors are identified |
| 1.8.1.12 | trypanothione-disulfide reductase |
pharmacology |
trypanothione reductase plays a central role in the trypanosomatid parasites defense against oxidative stress, trypanothione reductase is a promising target for antitrypanosomal drugs, synthesis of dethiotrypanothione and related trypanothione analogues featuring ring-closing olefin metathesis macrocyclizations is described |
| 1.11.1.7 | peroxidase |
pharmacology |
the enzyme is used as anticancer agent, which is verified by using three concentration of enzyme (0.010, 0.015, 0.020 mM/ml) which show a significant kill for Mcf-7 cells at (0.015 mg/ml), with cytotoxicity activity reaching (45%) |
| 1.13.11.6 | 3-hydroxyanthranilate 3,4-dioxygenase |
pharmacology |
the enzyme is a target for pharmacological downregulation because it is involved in formation of quinolinic acid, a highly potent excitotoxin implicated in a number of neurodegenerative conditions |
| 1.13.11.34 | arachidonate 5-lipoxygenase |
pharmacology |
human 5-lipoxygenase is a well-validated target for anti-inflammatory therapy. Development of 5-LOX inhibitors with higher activities is highly required |
| 1.13.11.52 | indoleamine 2,3-dioxygenase |
pharmacology |
first reaction in the tryptophan catabolic pathway in mammals |
| 1.13.11.52 | indoleamine 2,3-dioxygenase |
pharmacology |
IDO-1 is a target for pharmacological inhibition in the treatment of cancer |
| 1.13.11.55 | sulfur oxygenase/reductase |
pharmacology |
sulfur metabolism |
| 1.13.12.5 | Renilla-type luciferase |
pharmacology |
investigations into regulation and functional roles of kinases |
| 1.13.12.5 | Renilla-type luciferase |
pharmacology |
used as an assay for assessing potential liver toxicity by measuring GADD45-beta induction as an control for increased DNA damage |
| 1.14.11.11 | hyoscyamine (6S)-dioxygenase |
pharmacology |
tropane alkaloids including hyoscyamine, anisodamine, scopolamine and anisodine, are used medicinally as anticholinergic agents with increasing market demand, improvement of production by metabolic engineering introduction of genes encoding the branch-controlling enzyme tropinone reductase I and the downstream rate-limiting enzyme hyoscyamine-6beta-hydroxylase |
| 1.14.11.28 | proline 3-hydroxylase |
pharmacology |
the prolyl 3-hydroxylase P3H2 is a novel targets for epigenetic silencing in breast cancer |
| 1.14.11.28 | proline 3-hydroxylase |
pharmacology |
the prolyl 3-hydroxylase P3H3 is a novel targets for epigenetic silencing in breast cancer |
| 1.14.11.29 | hypoxia-inducible factor-proline dioxygenase |
pharmacology |
modulation of PHD2 activity might be considered as a new way to inhibit glioblastoma progression |
| 1.14.11.66 | [histone H3]-trimethyl-L-lysine9 demethylase |
pharmacology |
KDM4A possesses the potential to act as an oxygen sensor in the context of chromatin modifications, with possible implications for epigenetic regulation in hypoxic disease states |
| 1.14.13.9 | kynurenine 3-monooxygenase |
pharmacology |
kynurenine represents a branch point of the kynurenine pathway, being converted into the neurotoxin 3-hydroxykynurenine via kynurenine monooxygenase, neuroprotectant kynurenic acid, and anthranilic acid. As a result of this branch point, kynurenine monooxygenase is an attractive drug target for several neurodegenerative and/or neuroinflammatory diseases, especially Huntington's, Alzheimer's, and Parkinson's diseases |
| 1.14.13.9 | kynurenine 3-monooxygenase |
pharmacology |
the enzyme is a potential drug target for treatment of neurodegenerative disorders such as Huntington's and Alzheimer's diseases |
| 1.14.13.38 | anhydrotetracycline 6-monooxygenase |
pharmacology |
synthesis of chlortetracycline |
| 1.14.13.39 | nitric-oxide synthase (NADPH) |
pharmacology |
NO synthase can be used to gain insight into the biological role of endogenous agmatine |
| 1.14.13.64 | 4-hydroxybenzoate 1-hydroxylase |
pharmacology |
construction of a novel artificial pathway for arbutin biosynthesis in Escherichia colid. De novo biosynthesis of arbutin from simple carbon sources is established and a generalizable strategy for the biosynthesis of shikimate pathway derived chemicals is provided. Arbutin is a hydroquinone glucoside compound existing in various plants. It is widely used in pharmaceuticaland cosmetic industries owing to its well-known skin-lightening property as well as anti-oxidant, anti-microbial, and anti-inflammatory activities. A 4-hydroxybenzoate 1-hydroxylase gene from Candida parapsilosis CBS604 and a glucosyltransferase (arbutin synthase) gene from Rauvolfia serpentina are introduced into Escherichia coli lead to the production of 54.71 mg/l of arbutin from glucose. Further redirection of carbon flux into arbutin biosynthesis pathway by enhancing shikimate pathway genes enables production of 3.29 g/l arbutin, which is a 60-fold increase compared with the initial strain. Final optimization of glucose concentration added in the culture medium is able to further improve the titer of arbutin to 4.19 g/l in shake flasks experiments, which is around 77-fold higher than that of initial strain |
| 1.14.13.128 | 7-methylxanthine demethylase |
pharmacology |
methylxanthine intermediates of caffeine catabolism obtained by the action of N-demethylases have many applications. In medicine, theobromine and theophylline are used as diuretics, vasodilators, and myocardial stimulants. Monomethylxanthines can be converted to effective caffeine derivatives by chemical derivatization and hence can serve as interesting alternatives to caffeine. Xanthine also finds pharmaceutical application in drugs for treatment of asthma. The biotechnological potential of N-demethylases therefore lies not only in general decaffeination purposes but also in specific product recovery from caffeine |
| 1.14.14.17 | squalene monooxygenase |
pharmacology |
squalene epoxidase is an attractive potential target for drugs used to inhibit the growth of pathogenic fungi or to lower cholesterol level in humans |
| 1.14.14.83 | geraniol 8-hydroxylase |
pharmacology |
co-overexpression of geraniol-10-hydroxylase and strictosidine synthase improves anti-cancer drug camptothecin accumulation in Ophiorrhiza pumila |
| 1.14.14.91 | trans-cinnamate 4-monooxygenase |
pharmacology |
trans-cinnamate 4-monooxygenase plays a key role in the ability of phenylpropanoid metabolism to channel carbon to produce the 4-methoxybenzoyl group on the disaccharide moiety of OSW-1 (3beta,16beta,17alpha-trihydroxycholest-5-en-22-one 16-O-[O-[2-O-(4-methoxybenzoyl)-beta-D-xylopyranosyl]-(1->3)-2-O-acetyl-alpha-L-arabinopyranoside]). OSW-1 is about 10-100 times more cytotoxic than clinically applied anticanceragents such as mitomycin C, adriamycin, cisplatin, camptothecin, and paclitaxel, but has a low toxicity towards normal cells. This potency, in combination with a unique mechanism of action and selectivity toward malignant tumor cells, gives OSW-1 and its analogues great potential as anticancer agents |
| 1.14.14.92 | benzoate 4-monooxygenase |
pharmacology |
the enzyme is involved in detoxification of benzoate, a key intermediate in aromatic compound metabolism in fungi. Because this enzyme is unique to fungi, it is a promising drug target in fungal pathogens of other eukaryotes. By identifying selected derivatives of cinnamic acid as possible antifungal drugs, and CYP53 family enzymes as their targets, a potential inhibitor-target system for antifungal drugs is developed |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
- |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
target enzyme for azole antifungal agents. These specific inhibitors are of great importance as plant growth regulators, fungicides and herbicides in the agricultural and medical fields |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
all known functional sterols lack a 14alpha-methyl group, and therefore the 14alpha-demethylation reaction has received much attention from the pharmaceutical and agriculture-chemical industry as a possible means to specifically control and inhibit sterol biosynthesis in mammals, fungi, and plant |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
target for cholesterol-lowering drugs |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
target enzyme for the design of phyla-specific sterol 14alpha-demethylase inhibitors |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
CYP51 is a key target for fungal antibiotic therapy |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
Chagas disease is caused by the protozoan parasite Trypanosoma cruzi, which depends on the production of endogenous sterols, and therefore can be blocked by sterol 14alpha-demethylase inhibitors |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
the chemotherapy of leishmaniasis is a serious problem in the field of neglected tropical diseases. Since the biosynthesis of specific sterols is vital for effective survival, normal proliferation and infectivity of Leishmania parasites, the sterol 14alpha-demethylase inhibitors obtained from azole antifungal drug discovery programs can be used in antileishmanial therapy |
| 1.14.14.154 | sterol 14alpha-demethylase |
pharmacology |
the enzyme constitutes an important biological target for the most popular class of antifungals |
| 1.14.15.19 | C-19 steroid 1alpha-hydroxylase |
pharmacology |
modification at the C-1 position of a steroid is of pharmaceutical interest. Biotransformation can overcome tedious multistep chemical synthesis |
| 1.14.17.3 | peptidylglycine monooxygenase |
pharmacology |
enzyme is an attractive target for development of anti-tumor compounds |
| 1.14.18.1 | tyrosinase |
pharmacology |
(2R,3R)-taxifolin isolated from Benitade may possibly be a of new tyrosinase inhibitor alternative to cosmetic agents such as arbutin and kojic |
| 1.14.18.1 | tyrosinase |
pharmacology |
kurarinol, kuraridinol, and trifolirhizin are candidates as skin-whitening agents |
| 1.14.18.1 | tyrosinase |
pharmacology |
results indicate that the polyvinylpyrrolidone (PVP)-wrapped fullerene derivative (Radical Sponge) could be expected for its wide-ranged application as a whitening cosmetic material |
| 1.14.18.1 | tyrosinase |
pharmacology |
results of low cytotoxicity, high inhibition of melanin synthesis and lack of effect on gene expression suggest that p-hydroxybenzyl alcohol can be a potential agent for skin lightening to be used in cosmetic products |
| 1.14.18.1 | tyrosinase |
pharmacology |
study of suicide inactivation and irreversible inhibition is important in the functional design of synthetic inactivators for therapeutic applications |
