An imbalance in coagulation is associated with cardiovascular events. For prevention and treatment, anticoagulants, currently mainly xabans and gatrans, are used. The purpose of the present study was to provide a head-to-head comparison since there are no studies directly evaluating these novel anticoagulants. An additional aim was to find whether selected anthropological and biochemical factors can affect their anticoagulant properties as they are used in fixed doses. In this cross-sectional study, blood from 50 generally healthy donors was collected, and coagulation responses to dabigatran, argatroban, rivaroxaban, and apixaban, at a concentration of 1 μM, were analyzed. Heparin was used as a positive control. Prothrombin time (PT) expressed as international normalized ratio (INR) and activated partial thromboplastin time (aPTT) were measured and compared. Rivaroxaban was the most active according to PT/INR while argatroban according to aPTT. The ex vivo anticoagulant effect measured by INR correlated inversely with body mass index (BMI) in all four anticoagulants tested. Shortening of aPTT was associated with higher cholesterol and triglyceride levels. No sex-related differences were observed in response to the anticoagulant treatments. As this was an ex vivo study and pharmacokinetic factors were not included, the influence of BMI is of high therapeutic importance.

• Klíčová slova
• Activated partial thromboplastin time, Anticoagulants, Body mass index, Lipid, Prothrombin time,
• MeSH
• antikoagulancia * farmakologie   MeSH
• arginin * analogy a deriváty   MeSH
• dabigatran farmakologie   MeSH
• dospělí MeSH
• hemokoagulace * účinky léků   MeSH
• index tělesné hmotnosti MeSH
• INR MeSH
• kyseliny pipekolové * farmakologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladý dospělý MeSH
• parciální tromboplastinový čas MeSH
• protrombinový čas MeSH
• průřezové studie MeSH
• pyrazoly farmakologie   MeSH
• pyridony farmakologie   farmakokinetika   MeSH
• rivaroxaban * farmakologie   MeSH
• sulfonamidy farmakologie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• apixaban MeSH Prohlížeč
• argatroban MeSH Prohlížeč

Bruton's tyrosine kinase (BTK) is a promising molecular target for several human B-cell-related autoimmune disorders, inflammation, and haematological malignancies. The pathogenic alterations in various cancer tissues depend on mutant BTK for cell proliferation and survival, and BTK is also overexpressed in a range of hematopoietic cells. Due to this, BTK is emerging as a potential drug target to treat various human diseases, and several reversible and irreversible inhibitors have been developed and are being developed. As a result, BTK inhibition, clinically validated as an anticancer treatment, is finding great interest in B-cell malignancies and solid tumours. This study focuses on the design and synthesis of new oxindole sulfonamide derivatives as promising inhibitors of BTK with negligible off-target effects. The most cytotoxic compounds with greater basicity were PID-4 (2.29±0.52 μM), PID-6 (9.37±2.47 μM), and PID-19 (2.64±0.88 μM). These compounds caused a selective inhibition of Burkitt's lymphoma RAMOS cells without significant cytotoxicity in non-BTK cancerous and non-cancerous cell lines. Further, PID-4 showed promising activity in inhibiting BTK and downstream signalling cascades. As a potent inhibitor of Burkitt's lymphoma cells, PID-4 is a promising lead for developing novel chemotherapeutics.

• Klíčová slova
• Antiproliferation, B-cell malignancies, Bruton's tyrosine kinase, Cytotoxicity, Knoevenagel condensation, Oxindole sulfonamide,
• MeSH
• Burkittův lymfom * farmakoterapie   MeSH
• inhibitory proteinkinas MeSH
• inhibitory tyrosinkinasy * MeSH
• lidé MeSH
• proteinkinasa BTK MeSH
• sulfonamidy farmakologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• inhibitory proteinkinas MeSH
• inhibitory tyrosinkinasy * MeSH
• proteinkinasa BTK MeSH
• sulfonamidy MeSH

A series of 1,3,5-triazinyl aminobenzenesulfonamides substituted by aminoalcohol, aminostilbene, and aminochalcone structural motifs was synthesized as potential human carbonic anhydrase (hCA) inhibitors. The compounds were evaluated on their inhibition of tumor-associated hCA IX and hCA XII, hCA VII isoenzyme present in the brain, and physiologically important hCA I and hCA II. While the test compounds had only a negligible effect on physiologically important isoenzymes, many of the studied compounds significantly affected the hCA IX isoenzyme. Several compounds showed activity against hCA XII; (E)-4-{2-[(4-[(2,3-dihydroxypropyl)amino]-6-[(4-styrylphenyl)amino]-1,3,5-triazin-2-yl)amino]ethyl}benzenesulfonamide (31) and (E)-4-{2-[(4-[(4-hydroxyphenyl)amino]-6-[(4-styrylphenyl)amino]-1,3,5-triazin-2-yl)amino]ethyl}benzenesulfonamide (32) were the most effective inhibitors with KIs = 4.4 and 5.9 nM, respectively. In addition, the compounds were tested against vancomycin-resistant Enterococcus faecalis (VRE) isolates. (E)-4-[2-({4-[(4-cinnamoylphenyl)amino]-6-[(4-hydroxyphenyl)amino]-1,3,5-triazin-2-yl}amino)ethyl]benzenesulfonamide (21) (MIC = 26.33 µM) and derivative 32 (MIC range 13.80-55.20 µM) demonstrated the highest activity against all tested strains. The most active compounds were evaluated for their cytotoxicity against the Human Colorectal Tumor Cell Line (HCT116 p53 +/+). Only 4,4'-[(6-chloro-1,3,5-triazin-2,4-diyl)bis(iminomethylene)]dibenzenesulfonamide (7) and compound 32 demonstrated an IC50 of ca. 6.5 μM; otherwise, the other selected derivatives did not show toxicity at concentrations up to 50 µM. The molecular modeling and docking of active compounds into various hCA isoenzymes, including bacterial carbonic anhydrase, specifically α-CA present in VRE, was performed to try to outline a possible mechanism of selective anti-VRE activity.

• Klíčová slova
• benzenesulfonamide, carbonic anhydrase, chalcone, inhibition, stilbene, triazine, vancomycin-resistant enterococci,
• MeSH
• antibakteriální látky farmakologie   MeSH
• antitumorózní látky farmakologie   terapeutické užití   MeSH
• enterokoky rezistentní vůči vankomycinu účinky léků   MeSH
• HCT116 buňky MeSH
• inhibitory karboanhydras farmakologie   MeSH
• karboanhydrasa I antagonisté a inhibitory   MeSH
• karboanhydrasa II antagonisté a inhibitory   MeSH
• karboanhydrasa IX antagonisté a inhibitory   MeSH
• karboanhydrasy účinky léků   MeSH
• lidé MeSH
• nádory farmakoterapie   MeSH
• simulace molekulární dynamiky MeSH
• simulace molekulového dockingu MeSH
• sulfonamidy farmakologie   MeSH
• vztahy mezi strukturou a aktivitou MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antibakteriální látky MeSH
• antitumorózní látky MeSH
• carbonic anhydrase XII MeSH Prohlížeč
• inhibitory karboanhydras MeSH
• karboanhydrasa I MeSH
• karboanhydrasa II MeSH
• karboanhydrasa IX MeSH
• karboanhydrasy MeSH
• sulfonamidy MeSH

A current issue of antimicrobial therapy is the resistance to treatment with worldwide consequences. Thus, the identification of innovative targets is an intriguing challenge in the drug and development process aimed at newer antimicrobial agents. The state-of-art of anticholera therapy might comprise the reduction of the expression of cholera toxin, which could be reached through the inhibition of carbonic anhydrases expressed in Vibrio cholerae (VchCAα, VchCAβ, and VchCAγ). Therefore, we focused our interest on the exploitation of sulfonamides as VchCA inhibitors. We planned to design and synthesize new benzenesulfonamides based on our knowledge of the VchCA catalytic site. The synthesized compounds were tested thus collecting useful SAR information. From our investigation, we identified new potent VchCA inhibitors, some of them displayed high affinity toward VchCAγ class, for which few inhibitors are currently reported in literature. The best interesting VchCAγ inhibitor (S)-N-(1-oxo-1-((4-sulfamoylbenzyl)amino)propan-2-yl)furan-2-carboxamide (40) resulted more active and selective inhibitor when compared with acetazolamide (AAZ) as well as previously reported VchCA inhibitors.

• Klíčová slova
• Bacterial carbonic anhydrases, Drug Discovery, Enzymes Inhibitors, Sulfonamides, Vibrio cholerae,
• MeSH
• benzensulfonamidy MeSH
• inhibitory karboanhydras chemická syntéza   chemie   farmakologie   MeSH
• karboanhydrasy genetika   metabolismus   MeSH
• lidé MeSH
• molekulární modely MeSH
• molekulární struktura MeSH
• sulfonamidy chemická syntéza   chemie   farmakologie   MeSH
• Vibrio cholerae účinky léků   genetika   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• vztahy mezi strukturou a aktivitou MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• inhibitory karboanhydras MeSH
• karboanhydrasy MeSH
• sulfonamidy MeSH

Twelve novel analogs of STAT3 inhibitor BP-1-102 were designed and synthesised with the aim to modify hydrophobic fragments of the molecules that are important for interaction with the STAT3 SH2 domain. The cytotoxic activity of the reference and novel compounds was evaluated using several human and two mouse cancer cell lines. BP-1-102 and its two analogs emerged as effective cytotoxic agents and were further tested in additional six human and two murine cancer cell lines, in all of which they manifested the cytotoxic effect in a micromolar range. Reference compound S3I-201.1066 was found ineffective in all tested cell lines, in contrast to formerly published data. The ability of selected BP-1-102 analogs to induce apoptosis and inhibition of STAT3 receptor-mediated phosphorylation was confirmed. The structure-activity relationship confirmed a demand for two hydrophobic substituents, i.e. the pentafluorophenyl moiety and another spatially bulky moiety, for effective cytotoxic activity and STAT3 inhibition.

• Klíčová slova
• SH2 domain, STAT3 signalling pathway, cancer, inhibitor, structure–activity relationship,
• MeSH
• antitumorózní látky chemická syntéza   chemie   farmakologie   MeSH
• apoptóza účinky léků   MeSH
• fosforylace účinky léků   MeSH
• hydrofobní a hydrofilní interakce MeSH
• kultivované buňky MeSH
• kyseliny aminosalicylové chemická syntéza   chemie   farmakologie   MeSH
• lidé MeSH
• molekulární struktura MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• proliferace buněk účinky léků   MeSH
• racionální návrh léčiv * MeSH
• sulfonamidy chemická syntéza   chemie   farmakologie   MeSH
• transkripční faktor STAT3 antagonisté a inhibitory   metabolismus   MeSH
• viabilita buněk účinky léků   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• vztahy mezi strukturou a aktivitou MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antitumorózní látky MeSH
• BP-1-102 MeSH Prohlížeč
• kyseliny aminosalicylové MeSH
• STAT3 protein, human MeSH Prohlížeč
• sulfonamidy MeSH
• transkripční faktor STAT3 MeSH

Background: Increasing resistance has resulted in an urgent need for new antimicrobial drugs. A systematic me-too approach was chosen to modify clinically used sulfonamides to obtain their imines. Methods & results: Twenty-five compounds were synthesized and evaluated for their antibacterial activity. The most active compounds were also investigated against methicillin- and trimethoprim/sulfamethoxazole (SMX)-resistant Gram-positive species. Staphylococci shared the highest susceptibility including resistant strains with minimum inhibitory concentrations from 3.91 μM (≥2.39 μg ml-1). Crucially, the compounds inhibit MRSA and trimethoprim/SMX-resistant Staphylococci without any cross-resistance. Modification of parent sulfonamides turned a bacteriostatic effect into a bactericidal effect. Toxicity for HepG2 and hemolytic properties were also determined. Conclusions: The presence of a dihalogenated salicylidene moiety is required for optimal activity. Based on toxicity, promising derivatives for further investigation were identified.

• Klíčová slova
• Schiff bases, Staphylococcus aureus, antibacterial activity, cytotoxicity, drug resistance, imine, in vitro activity, sulfamethoxazole, sulfonamides,
• MeSH
• aldehydy chemie   farmakologie   MeSH
• antibakteriální látky chemická syntéza   chemie   farmakologie   MeSH
• bakteriální léková rezistence účinky léků   MeSH
• iminy chemie   farmakologie   MeSH
• mikrobiální testy citlivosti MeSH
• molekulární struktura MeSH
• Staphylococcus účinky léků   MeSH
• sulfonamidy chemie   farmakologie   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• aldehydy MeSH
• antibakteriální látky MeSH
• iminy MeSH
• salicylaldehyde MeSH Prohlížeč
• sulfonamidy MeSH

BACKGROUND: Unconjugated hyperbilirubinemia, a feature of neonatal jaundice or Crigler-Najjar syndrome, can lead to neurotoxicity and even death. We previously demonstrated that unconjugated bilirubin (UCB) can be eliminated via transintestinal excretion in Gunn rats, a model of unconjugated hyperbilirubinemia, and that this is stimulated by enhancing fecal fatty acid excretion. Since transintestinal excretion also occurs for cholesterol (TICE), we hypothesized that increasing fecal cholesterol excretion and/or TICE could also enhance fecal UCB disposal and subsequently lower plasma UCB concentrations. METHODS: To determine whether increasing fecal cholesterol excretion could ameliorate unconjugated hyperbilirubinemia, we treated hyperbilirubinemic Gunn rats with ezetimibe (EZE), an intestinal cholesterol absorption inhibitor, and/or a liver X receptor (LXR) and farnesoid X receptor (FXR) agonist (T0901317 (T09) and obeticholic acid (OCA), respectively), known to stimulate TICE. RESULTS: We found that EZE treatment alone or in combination with T09 or OCA increased fecal cholesterol disposal but did not lower plasma UCB levels. CONCLUSIONS: These findings do not support a link between the regulation of transintestinal excretion of cholesterol and bilirubin. Furthermore, induction of fecal cholesterol excretion is not a potential therapy for unconjugated hyperbilirubinemia. IMPACT: Increasing fecal cholesterol excretion is not effective to treat unconjugated hyperbilirubinemia. This is the first time a potential relation between transintestinal excretion of cholesterol and unconjugated bilirubin is investigated. Transintestinal excretion of cholesterol and unconjugated bilirubin do not seem to be quantitatively linked. Unlike intestinal fatty acids, cholesterol cannot "capture" unconjugated bilirubin to increase its excretion. These results add to our understanding of ways to improve and factors regulating unconjugated bilirubin disposal in hyperbilirubinemic conditions.

• MeSH
• bilirubin chemie   MeSH
• cholesterol metabolismus   MeSH
• Criglerův-Najjarův syndrom metabolismus   terapie   MeSH
• dietní tuky farmakokinetika   MeSH
• ezetimib farmakologie   terapeutické užití   MeSH
• feces chemie   MeSH
• fluorované uhlovodíky farmakologie   terapeutické užití   MeSH
• haptoglobiny analýza   MeSH
• hyperbilirubinemie terapie   MeSH
• jaterní receptor X metabolismus   MeSH
• krysa rodu Rattus MeSH
• kyselina chenodeoxycholová analogy a deriváty   farmakologie   terapeutické užití   MeSH
• lipidy krev   MeSH
• náhodné rozdělení MeSH
• potkani Gunn MeSH
• PPAR delta metabolismus   MeSH
• receptory cytoplazmatické a nukleární metabolismus   MeSH
• střeva účinky léků   metabolismus   MeSH
• sulfonamidy farmakologie   terapeutické užití   MeSH
• žluč chemie   MeSH
• žlučové kyseliny a soli metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• bilirubin MeSH
• cholesterol MeSH
• dietní tuky MeSH
• ezetimib MeSH
• farnesoid X-activated receptor MeSH Prohlížeč
• fluorované uhlovodíky MeSH
• haptoglobiny MeSH
• jaterní receptor X MeSH
• kyselina chenodeoxycholová MeSH
• lipidy MeSH
• obeticholic acid MeSH Prohlížeč
• PPAR delta MeSH
• receptory cytoplazmatické a nukleární MeSH
• sulfonamidy MeSH
• T0901317 MeSH Prohlížeč
• žlučové kyseliny a soli MeSH

Human carbonic anhydrase IX (CA IX), a protein specifically expressed on the surface of solid tumour cells, represents a validated target both for anticancer therapy and diagnostics. We recently identified sulfonamide dicarbaboranes as promising inhibitors of CA IX with favourable activities both in vitro and in vivo. To explain their selectivity and potency, we performed detailed X-ray structural analysis of their interactions within the active sites of CA IX and CA II. Series of compounds bearing various aliphatic linkers between the dicarbaborane cluster and sulfonamide group were examined. Preferential binding towards the hydrophobic part of the active site cavity was observed. Selectivity towards CA IX lies in the shape complementarity of the dicarbaborane cluster with a specific CA IX hydrophobic patch containing V131 residue. The bulky side chain of F131 residue in CA II alters the shape of the catalytic cavity, disrupting favourable interactions of the spherical dicarbaborane cluster.

• Klíčová slova
• Carbonic anhydrase IX, carborane, enzyme inhibitors, structure-activity relationship,
• MeSH
• antigeny nádorové genetika   MeSH
• antitumorózní látky chemie   farmakologie   MeSH
• HEK293 buňky MeSH
• hydrofobní a hydrofilní interakce MeSH
• inhibitory karboanhydras chemie   farmakologie   MeSH
• karboanhydrasa IX antagonisté a inhibitory   genetika   MeSH
• katalytická doména MeSH
• krystalografie rentgenová MeSH
• léky antitumorózní - screeningové testy MeSH
• lidé MeSH
• sekvence aminokyselin MeSH
• sloučeniny boru chemie   MeSH
• sulfonamidy chemie   farmakologie   MeSH
• vazba proteinů MeSH
• vztahy mezi strukturou a aktivitou MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antigeny nádorové MeSH
• antitumorózní látky MeSH
• CA9 protein, human MeSH Prohlížeč
• decaborane MeSH Prohlížeč
• inhibitory karboanhydras MeSH
• karboanhydrasa IX MeSH
• sloučeniny boru MeSH
• sulfonamidy MeSH

AIMS: To demonstrate the bioequivalence of macitentan/tadalafil fixed-dose combination (FDC) tablets with single-component tablets of macitentan and tadalafil in healthy subjects. METHODS: Studies AC-077-101 and AC-077-103 were single-centre, open-label, single-dose, 2-period, randomized, crossover Phase 1 studies conducted in healthy subjects. Two FDCs were investigated: FDC-1 and FDC-2 in Study AC-077-101 and FDC-2 in Study AC-077-103. Both FDCs contained 10 mg/40 mg of macitentan/tadalafil and differed in excipients and coating materials used. In both studies, pharmacokinetic sampling over 216 hours was conducted, and pharmacokinetic parameters were derived using noncompartmental methods. RESULTS: Bioequivalence of macitentan, its active metabolite ACT-132577, and tadalafil was established for FDC-2 in both studies AC-077-101 and AC-077-103 in which tadalafil as a single component was sourced from the USA and EU, respectively, to fulfil regional regulatory requirements. The area under the plasma concentration-time curve and maximum plasma concentration with 90% confidence intervals of all components were entirely within the bioequivalence limits (0.8000-1.2500). No subject died and no serious adverse events were reported in either studies. CONCLUSION: The FDC-2 tablet containing 10 mg/40 mg of macitentan/tadalafil was bioequivalent to the free combination of 10 mg macitentan and 40 mg tadalafil (both US and EU sourced). Macitentan and tadalafil were well tolerated when administered as FDC or as a free combination.

• Klíčová slova
• bioequivalence, fixed-dose combination, macitentan, pulmonary arterial hypertension, tadalafil,
• MeSH
• dospělí MeSH
• fixní kombinace léků MeSH
• hypoglykemika * farmakologie   MeSH
• klinické křížové studie MeSH
• léky s prodlouženým účinkem MeSH
• lidé středního věku MeSH
• lidé MeSH
• metformin * MeSH
• mladiství MeSH
• mladý dospělý MeSH
• plocha pod křivkou MeSH
• pyrimidiny * farmakologie   MeSH
• sulfonamidy * farmakologie   MeSH
• tablety MeSH
• tadalafil * farmakologie   MeSH
• terapeutická ekvivalence MeSH
• zdraví dobrovolníci pro lékařské studie MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• fixní kombinace léků MeSH
• hypoglykemika * MeSH
• léky s prodlouženým účinkem MeSH
• macitentan MeSH Prohlížeč
• metformin * MeSH
• pyrimidiny * MeSH
• sulfonamidy * MeSH
• tablety MeSH
• tadalafil * MeSH

The identification of the essential role of cyclin-dependent kinases (CDKs) in the control of cell division has prompted the development of small-molecule CDK inhibitors as anticancer drugs. For many of these compounds, the precise mechanism of action in individual tumor types remains unclear as they simultaneously target different classes of CDKs - enzymes controlling the cell cycle progression as well as CDKs involved in the regulation of transcription. CDK inhibitors are also capable of activating p53 tumor suppressor in tumor cells retaining wild-type p53 gene by modulating MDM2 levels and activity. In the current study, we link, for the first time, CDK activity to the overexpression of the MDM4 (MDMX) oncogene in cancer cells. Small-molecule drugs targeting the CDK9 kinase, dinaciclib, flavopiridol, roscovitine, AT-7519, SNS-032, and DRB, diminished MDM4 levels and activated p53 in A375 melanoma and MCF7 breast carcinoma cells with only a limited effect on MDM2. These results suggest that MDM4, rather than MDM2, could be the primary transcriptional target of pharmacological CDK inhibitors in the p53 pathway. CDK9 inhibitor atuveciclib downregulated MDM4 and enhanced p53 activity induced by nutlin-3a, an inhibitor of p53-MDM2 interaction, and synergized with nutlin-3a in killing A375 melanoma cells. Furthermore, we found that human pluripotent stem cell lines express significant levels of MDM4, which are also maintained by CDK9 activity. In summary, we show that CDK9 activity is essential for the maintenance of high levels of MDM4 in human cells, and drugs targeting CDK9 might restore p53 tumor suppressor function in malignancies overexpressing MDM4.

• MeSH
• cyklin-dependentní kinasa 9 antagonisté a inhibitory   metabolismus   MeSH
• genetická transkripce MeSH
• imidazoly farmakologie   MeSH
• inhibitory proteinkinas farmakologie   MeSH
• lidé MeSH
• melanom genetika   metabolismus   patologie   MeSH
• MFC-7 buňky MeSH
• myši MeSH
• nádorové buněčné linie MeSH
• nádory prsu genetika   metabolismus   patologie   MeSH
• piperaziny farmakologie   MeSH
• pluripotentní kmenové buňky metabolismus   MeSH
• proteiny buněčného cyklu biosyntéza   genetika   metabolismus   MeSH
• protoonkogenní proteiny c-mdm2 biosyntéza   genetika   metabolismus   MeSH
• protoonkogenní proteiny biosyntéza   genetika   metabolismus   MeSH
• roskovitin farmakologie   MeSH
• sulfonamidy farmakologie   MeSH
• synergismus léků MeSH
• transfekce MeSH
• triaziny farmakologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• atuveciclib MeSH Prohlížeč
• CDK9 protein, human MeSH Prohlížeč
• Cdk9 protein, mouse MeSH Prohlížeč
• cyklin-dependentní kinasa 9 MeSH
• imidazoly MeSH
• inhibitory proteinkinas MeSH
• MDM2 protein, human MeSH Prohlížeč
• Mdm2 protein, mouse MeSH Prohlížeč
• MDM4 protein, human MeSH Prohlížeč
• Mdm4 protein, mouse MeSH Prohlížeč
• nutlin 3 MeSH Prohlížeč
• piperaziny MeSH
• proteiny buněčného cyklu MeSH
• protoonkogenní proteiny c-mdm2 MeSH
• protoonkogenní proteiny MeSH
• roskovitin MeSH
• sulfonamidy MeSH
• triaziny MeSH