Viable crystals of ERK2 were briefly transferred into a cryo-protectant made from the crystallization mother liquor supplemented with 22% ethylene glycol, while this step was not required for the soaked ERK1 and JNK1 crystals and haspin co-crystals. All crystals were flash-cooled in liquid nitrogen, and diffraction data were collected at Diamond Light Source and processed with MOSFLM50 (link) before subsequent scaling using SCALA51 (link) from CCP4 suite52 (link). Molecular replacement was performed for structure solutions using Phaser program53 (link) and the kinase coordinates of ERK1-5-iodotubercidin complex28 (link), inactive ERK220 (link), haspin-AMP complex23 (link) and JNK1-inhibitor complex54 (link) as search models for ERK1, ERK2, haspin and JNK1, respectively. All structures were subjected to iterative cycles of manual model building in COOT55 (link) alternated with refinement using REFMAC56 (link). TLS definitions used in the late refinement step were calculated using TLSMD server57 (link). Geometric correctness of all kinase-SCH772984 complexes was validated with MOLPROBITY58 (link). Statistics for data collection and structure refinement are summarized in Supplementary Table 1 .
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Chemicals & Drugs
>
Organic Chemical
>
SCH772984
SCH772984
SCH772984 is a potent and selective inhibitor of the PI3K/mTOR signaling pathway, which plays a crucial role in regulating cell growth, proliferation, and survival.
This compound has been extensively studied for its potential therapeutic applications in various disease states, including cancer, neurological disorders, and metabolic conditions.
PubCompare.ai, the leading AI-driven platform, can help optimize your SCH772984 research by providing access to protocols from literature, pre-prints, and patents, as well as leveraging AI-driven comparisons to identify the best protocols and products.
Streamline your SCH772984 research with PubCompare.ai's powerful tools and expertise, and enhance the reproducibility and accuracy of your findings.
This compound has been extensively studied for its potential therapeutic applications in various disease states, including cancer, neurological disorders, and metabolic conditions.
PubCompare.ai, the leading AI-driven platform, can help optimize your SCH772984 research by providing access to protocols from literature, pre-prints, and patents, as well as leveraging AI-driven comparisons to identify the best protocols and products.
Streamline your SCH772984 research with PubCompare.ai's powerful tools and expertise, and enhance the reproducibility and accuracy of your findings.
Most cited protocols related to «SCH772984»
Amniotic Fluid
Crystallization
Diamond
Glycol, Ethylene
Light
Mitogen-Activated Protein Kinase 3
Mitogen Activated Protein Kinase 1
Mothers
Nitrogen
Phosphotransferases
Protective Agents
SCH772984
Anophthalmia with pulmonary hypoplasia
Cell Lines
Cells
Centrifugation
Cloning Vectors
Common Cold
Freezing
Genes
Homo sapiens
K-ras Genes
mRNA, Polyadenylated
Oligonucleotide Primers
Oligonucleotides
Pancreas
RNA-Seq
Salmo salar
SCH772984
Short Hairpin RNA
Alleles
Arm, Upper
Biopharmaceuticals
Cells
Chimera
Cloning Vectors
Division, Cell
DNA Library
DNA Replication
Doxycycline
Endoribonucleases
Genome
Infection
Mitogen Activated Protein Kinase 1
Oligonucleotide Primers
Pellets, Drug
Phenotype
Puromycin
SCH772984
Protocol full text hidden due to copyright restrictions
Open the protocol to access the free full text link
Acetylcysteine
Actins
Antibodies
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
Biological Assay
Biological Factors
BODIPY
Cell Survival
CTNNB1 protein, human
cupric chloride
Cycloheximide
DAPI
Deferoxamine
Disulfiram
Esters
ferrostatin-1
GAPDH protein, human
GSK3B protein, human
Helix (Snails)
Immunoglobulins
MG 132
N-Cadherins
NAD(P)H dehydrogenase (quinone) 1, human
NFE2L2 protein, human
Novus
rhodamine B
SB 203580
SCH772984
Sorafenib
SP600125
trigonelline
Vimentin
All mouse experiments have been regulated under the Animals (Scientific Procedures) Act 1986 Amendment Regulations 2012 following ethical review by the University of Cambridge Animal Welfare and Ethical Review Body (AWERB) and have been performed in accordance to the Home Office license awarded to M.H. For subcutaneous grafts, 1 million cells suspensions were prepared in PBS-0.1%BSA (CC and healthy liver-derived organoid lines) or in Advanced DMEM/F12 (GIBCO) 1% glycosil (ESI-BIO) further supplemented with 50 ng/ml each of HGF and VEGF (HCC and healthy liver-derived organoid lines) and were injected into both flanks of male NSG-NOD scid gamma mice (Charles River). Visible tumours developed in approximately 2–4 weeks (CC organoid lines) and 4-6 months (HCC-1 organoid line). Mice were culled when the tumour reached limit end-point (size or ulceration). For kidney capsule graft, cell line suspensions were prepared in Advanced DMEM/F12 (GIBCO) with BME2 (7mg/ml) and 500.000 cells were implanted under the renal capsule of NSG mice. These mice were then culled at different time point (0.5, 1, 2 and 3 month) and kidney and lung tissues were harvested to assess the growth and the metastatic potential of the grafted cells.
To assess the efficiency of the ERK inhibitor SCH772984 in vivo mice with established subcutaneous tumours were randomized to drug treatment by splitting size-matched tumours in two groups (SCH772984/vehicle). Treatments (SCH772984 at 2 mg/kg, or an equal volume of vehicle (25%DMSO-30%PEG300 in DD water) were administered by intratumoural injection twice daily for 15 (CC-1 tumouroid line) or 20 (HCC-1 tumouroid line) days. Tumour sizes were measured 3 times a week after the first week of treatment using a caliper and volumes were calculated by applying the formula v = 0.5 × L × w × h, where v is volume, L is length, w is width and h is height. Investigators performing tumour measurements were blinded to treatment groups. Histological analyses of the tumours from both CC-1 and HCC-1 lines were performed at 24 and 25 days after treatment initiation respectively.
To assess the efficiency of the ERK inhibitor SCH772984 in vivo mice with established subcutaneous tumours were randomized to drug treatment by splitting size-matched tumours in two groups (SCH772984/vehicle). Treatments (SCH772984 at 2 mg/kg, or an equal volume of vehicle (25%DMSO-30%PEG300 in DD water) were administered by intratumoural injection twice daily for 15 (CC-1 tumouroid line) or 20 (HCC-1 tumouroid line) days. Tumour sizes were measured 3 times a week after the first week of treatment using a caliper and volumes were calculated by applying the formula v = 0.5 × L × w × h, where v is volume, L is length, w is width and h is height. Investigators performing tumour measurements were blinded to treatment groups. Histological analyses of the tumours from both CC-1 and HCC-1 lines were performed at 24 and 25 days after treatment initiation respectively.
Aftercare
Animals
Capsule
Cell Lines
Cells
Cell Transplants
Ethical Review
Gamma Rays
Grafts
Human Body
Kidney
Kidney Transplantation
Liver
Lung
Males
Mice, Inbred NOD
Mus
Neoplasms
Organoids
Pharmaceutical Preparations
polyethylene glycol 300
Rivers
SCH772984
SCID Mice
Sulfoxide, Dimethyl
Tissues
Ulcer
Vascular Endothelial Growth Factors
Most recents protocols related to «SCH772984»
SHP099, LXH254, and ribociclib (LEE011) were provided by the Novartis Institutes of Biomedical Research. Lapatinib (catalog L-4804) was purchased from LC Laboratories. Bosutinib, defactinib, SCH772984, and trametinib were purchased from Selleck Chemicals. All inhibitors were dissolved in DMSO before use.
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bosutinib
defactinib
inhibitors
Lapatinib
LEE011
ribociclib
SCH772984
SHP099
Sulfoxide, Dimethyl
trametinib
Dulbecco’s PBS, DMEM, McCoy’s 5A (Modified) Medium, Opti-MEM I Reduced Serum Medium, sodium pyruvate (100 mM), penicillin–streptomycin (PenStrep, 10,000 U/ml penicillin, 10,000 μg/ml streptomycin), puromycin (10 mg/ml), Lipofectamine LTX Reagent with PLUS Reagent, PageRuler Prestained Protein Ladder, Spectra Multicolor High Range Protein Ladder, propidium iodide (PI), trypsin–EDTA solution (TE), Power SYBR Green PCR Master Mix, DNase I, RNase A (10 mg/ml), High-Capacity RNA-to-cDNA Kit, TRIzol, and the Pierce BCA Protein Assay Kit were purchased from Thermo Fisher Scientific or their associated companies Invitrogen or Applied Biosystems. Fetal calf serum (FCS) was obtained from Capricorn Scientific GmbH. PhosSTOP, cOmplete Mini (from Roche), MISSION shRNA pLKO.1-vectors, MEM non-essential amino acid solution (100×), polybrene, polyethylene glycol (PEG8000), polyethylenimine (PEI), coenzyme A (lithium salt), sodium hydrosulfite (Na2S2O4), and adenosine 5′-monophosphate (disodium salt; AMP) were obtained from Sigma-Aldrich. Tris(hydroxymethyl)aminomethane (Tris), Tween-20, Triton X-100, Hepes, DTT, magnesium sulfate (MgSO2), and sodium dodecyl sulfate were bought from PanReac AppliChem ITW Reagents. Sodium chloride (NaCl) and ethanol were purchased from Carl Roth. NEBuilder HiFi DNA Assembly Master Mix and all restriction enzymes used were purchased from New England Biolabs, Inc. Primers were obtained from Eurofins Scientific SE. Peroxide-free ARA, butylhydroxytoluol, cobimetinib, dactolisib, erlotinib, HLM006474, LB42708, PD184352, SCH772984, temsirolimus, pifithrin-ɑ, NSC68811, and wortmannin were purchased from Cayman Chemical Company. Palbociclib and Ro-3306 were purchased by MedChemExpress. EDTA (Titriplex III) and ɑ-D-glucose were purchased from Merck KGaA. Adenosine 5′-triphosphate (disodium salt; ATP) and calcium chloride were obtained from Carl Roth GmbH + Co. KG. Beetle luciferin (potassium salt; D-luciferin) was purchased from Promega Corporation.
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Adenosine Monophosphate
Adenosine Triphosphate
Amino Acids, Essential
Beetles
Biological Assay
Caimans
Calcium chloride
Cloning Vectors
cobimetinib
Coenzyme A
dactolisib
Deoxyribonuclease I
DNA, Complementary
DNA Restriction Enzymes
Edetic Acid
Erlotinib
Ethanol
Fetal Bovine Serum
Glucose
HEPES
HLM006474
LB42708
Lipofectamine
Lithium
Luciferins
methylamine
Oligonucleotide Primers
palbociclib
PD 184352
Penicillins
Peroxides
pifithrin
Polybrene
polyethylene glycol 8000
Polyethylene Glycols
Polyethyleneimine
Potassium
Promega
Propidium Iodide
Proteins
Puromycin
Pyruvate
Ribonucleases
RO 3306
SCH772984
Serum
Short Hairpin RNA
Sodium
Sodium Chloride
sodium hydrogen sulfite
Streptomycin
Sulfate, Magnesium
Sulfate, Sodium Dodecyl
SYBR Green I
temsirolimus
Triton X-100
trizol
Tromethamine
Trypsin
Tween 20
Wortmannin
MCs were isolated from human foreskin tissue as previously described [51 (link)]. Each mast cell preparation/culture originated from several (2–10) donors to achieve sufficient cell numbers, as routinely performed in our lab [52 (link),53 (link),57 (link),88 (link),89 (link)]. The skin was obtained from circumcisions, with written, informed consent of the patients or legal guardians and approval by the university ethics committee (protocol code EA1/204/10, 9 March 2018). The experiments were conducted according to the Declaration of Helsinki Principles. Briefly, the skin was cut into strips and treated with dispase (26.5 mL per preparation, activity: 3.8 U/mL; Boehringer-Mannheim, Mannheim, Germany) at 4 °C overnight, the epidermis was removed, the dermis was finely chopped and then digested with 2.29 mg/mL collagenase (activity: 255 U/mg; Worthington, Lakewood, NJ, USA), 0.75 mg/mL hyaluronidase (activity: 1000 U/mg; Sigma, Deisenhofen, Germany) and DNase I at 10 µg/mL (Roche, Basel, Switzerland). Cells were filtered stepwise from the resulting suspension (100 and 40 µm strainers, Fisher Scientific, Berlin, Germany). MC purification was achieved by anti-human c-Kit microbeads (#130-091-332) and an Auto-MACS separation device (both from Miltenyi-Biotec, Bergisch Gladbach, Germany), giving rise to 98–100% pure preparations (FACS double staining of KIT/FcεRI (anti-FcεRI eBiosciene #11-5899-42), Fisher Scientific; anti-CD117 Miltenyi-Biotec # 130-111-593) and acidic toluidine blue (Sigma) staining, 0.1% in 0.5 N HCl (Fisher Scientific), as described previously [90 (link),91 (link)].
MCs were cultured in the presence of SCF, and IL-4 was freshly provided twice weekly when cultures were re-adjusted to 5 × 105/mL. MCs were automatically counted by CASY-TTC (Innovatis/Casy Technology, Reutlingen, Germany) [88 (link),92 (link)].
Experiments were performed 3–4 d after the last addition of growth factors. For inhibition studies, cells were pre-incubated with 666-15 (CREB inhibitor; 5 µM unless otherwise stated; from Merck Chemicals, Darmstadt, Germany) or SCH772984 (ERK1/2 inhibitor; 10 µM), Pictilisib (PI3K inhibitor; 10 µM), Trametinib (MEK1/2 inhibitor; 10 µM), SB203580 (p38 inhibitor; 10 µM), SP600125 (JNK inhibitor; 10 µM), Pimozide (STAT5 inhibitor; 10 µM) and STAT3-IN (STAT3 inhibitor; 10 µM), all from Enzo Life Sciences, Germany, or imatinib-mesylate (Gleevec, KIT inhibitor; 10 µM, from Biozol Diagnostica, Eching, Germany) or KT 5720 (PKA inhibitor; 2 µM, from Bio-Techne, Wiesbaden, Germany) for 15 min, then stimulated (or not) by SCF (100 ng/mL). IL-33 was purchased from PeproTech (Hamburg, Germany) and applied in a concentration of 20 ng/mL, as described previously [52 (link)].
MCs were cultured in the presence of SCF, and IL-4 was freshly provided twice weekly when cultures were re-adjusted to 5 × 105/mL. MCs were automatically counted by CASY-TTC (Innovatis/Casy Technology, Reutlingen, Germany) [88 (link),92 (link)].
Experiments were performed 3–4 d after the last addition of growth factors. For inhibition studies, cells were pre-incubated with 666-15 (CREB inhibitor; 5 µM unless otherwise stated; from Merck Chemicals, Darmstadt, Germany) or SCH772984 (ERK1/2 inhibitor; 10 µM), Pictilisib (PI3K inhibitor; 10 µM), Trametinib (MEK1/2 inhibitor; 10 µM), SB203580 (p38 inhibitor; 10 µM), SP600125 (JNK inhibitor; 10 µM), Pimozide (STAT5 inhibitor; 10 µM) and STAT3-IN (STAT3 inhibitor; 10 µM), all from Enzo Life Sciences, Germany, or imatinib-mesylate (Gleevec, KIT inhibitor; 10 µM, from Biozol Diagnostica, Eching, Germany) or KT 5720 (PKA inhibitor; 2 µM, from Bio-Techne, Wiesbaden, Germany) for 15 min, then stimulated (or not) by SCF (100 ng/mL). IL-33 was purchased from PeproTech (Hamburg, Germany) and applied in a concentration of 20 ng/mL, as described previously [52 (link)].
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Acids
Cell Culture Techniques
Cells
Deoxyribonuclease I
Dermis
dispase
Donors
Epidermis
Ethics Committees
Factor D, Complement
Fc epsilon RI
Foreskin
Gleevec
Homo sapiens
Hyaluronidase
IL33 protein, human
Imatinib Mesylate
KT 5720
Legal Guardians
Male Circumcision
MAP2K1 protein, human
Medical Devices
Microspheres
Mitogen-Activated Protein Kinase 3
Neutrophil Collagenase
Patients
Phosphatidylinositol 3-Kinases
pictilisib
Pimozide
PKA inhibitor
Psychological Inhibition
SB 203580
SCH772984
Skin
SP600125
STAT3 Protein
STAT5A protein, human
Tissues
Tolonium Chloride
trametinib
B-ALL cell lines (NALM6 and RS4;11) and NALM6 phospho-GR mutants (GR-S203A and GR-S226A) were tested with combinations of prednisolone (Acros Organics, #449470250) and the PI3Kδ inhibitor idelalisib (Gilead). Viability was measured using PrestoBlue (ThermoFisher, A13262). Synergy was evaluated using the Bliss synergy model in SynergyFinder 2.0 (19 (link)).
Primary specimens from children with newly diagnosed or relapsed B-ALL were obtained after receiving informed consent (University of Iowa IRB protocol #201707711). Cells were isolated by Histopaque density gradient separation.
NALM6, SUP-B15, and RCH-ACV cells were tested with dexamethasone (Sigma, D4902–1g) in combination with ERK1/2 inhibitor SCH772984 (SelleckChem, #S7101).
Primary specimens from children with newly diagnosed or relapsed B-ALL were obtained after receiving informed consent (University of Iowa IRB protocol #201707711). Cells were isolated by Histopaque density gradient separation.
NALM6, SUP-B15, and RCH-ACV cells were tested with dexamethasone (Sigma, D4902–1g) in combination with ERK1/2 inhibitor SCH772984 (SelleckChem, #S7101).
Burkitt Leukemia
Cell Lines
Cells
Child
Dexamethasone
histopaque
idelalisib
Mitogen-Activated Protein Kinase 3
Prednisolone
SCH772984
Four CPP apparatuses each consisting of two equal compartments (15 cm × 15 cm × 37 cm) were used in this study. One was a white compartment with a metal grid floor and the other was a black compartment with a metal mesh floor. A movable baffle was in the center of apparatus. During the test period, the mice was allowed to shuttle freely in the apparatus by opening the baffle, and during training period, the mice was restricted to one side of the apparatus by closing the baffle. In this study, pre‐test results showed that mice spent more time in the black compartment than in the white compartment. Therefore, the black compartment was the “preferred‐one” and the white compartment was the “non‐preferred‐one”.
On day1, mice were pre‐tested for 15 min. Mice with abnormal activity (low motor activity, <20 shuttles, or more than 600 s spent on either side) were excluded.
In the acquisition phase (days 2–9), on days 2, 4, 6, and 8, all groups were injected with saline and placed in the black compartment for 45 min. On days 3, 5, 7, and 9, the control group was injected with saline; the drug group was injected with 1 mg/kg psilocin, 2 mg/kg TFP‐2HCl, or 10 mg/kg SCH772984; the METH group was injected with METH; and the METH with drug intervention group was injected with 1 mg/kg psilocin, 2 mg/kg TFP‐2HCl, or 10 mg/kg SCH772984 30 min before METH administration. All groups were placed in the white compartment for 45 min. At post‐test (day 10), all mice were allowed to explore the two compartments freely for 15 min.
In the extinction phase (days 11–22), four groups including control, PI, METH‐Ext1, and METH‐Ext2 were subjected to extinction training and testing. The METH group with CPP was divided into METH‐Ext1 and METH‐Ext2 groups. On day 11, four groups were injected with saline and placed in the black compartment for 45 min. On day 12, the control and METH‐Ext1 groups were injected with saline; PI and METH‐Ext2 groups were injected with psilocin, and all groups were placed in the white compartment for 45 min. On day 13, all mice were allowed to explore the two compartments freely for 15 min. This procedure was repeated three times over days 14–22.
In the reinstatement phase, four groups including Control, PI, METH‐Rein1 and METH‐Rein2 were tested. The METH‐Ext1 group was divided into METH‐Rein1 and METH‐Rein2 groups. The METH‐Rein1 group was injected (i.p) with METH, and the METH‐Rein2 group was injected (i.p) with 1 mg/kg psilocin prior to METH injections. The mice were then allowed to explore the two compartments freely for 15 min. At the end of the experimentation, the mice were sacrificed, and the PFC, NAc, and VTA were collected. Samples were stored at −80°C until subsequent use.
On day1, mice were pre‐tested for 15 min. Mice with abnormal activity (low motor activity, <20 shuttles, or more than 600 s spent on either side) were excluded.
In the acquisition phase (days 2–9), on days 2, 4, 6, and 8, all groups were injected with saline and placed in the black compartment for 45 min. On days 3, 5, 7, and 9, the control group was injected with saline; the drug group was injected with 1 mg/kg psilocin, 2 mg/kg TFP‐2HCl, or 10 mg/kg SCH772984; the METH group was injected with METH; and the METH with drug intervention group was injected with 1 mg/kg psilocin, 2 mg/kg TFP‐2HCl, or 10 mg/kg SCH772984 30 min before METH administration. All groups were placed in the white compartment for 45 min. At post‐test (day 10), all mice were allowed to explore the two compartments freely for 15 min.
In the extinction phase (days 11–22), four groups including control, PI, METH‐Ext1, and METH‐Ext2 were subjected to extinction training and testing. The METH group with CPP was divided into METH‐Ext1 and METH‐Ext2 groups. On day 11, four groups were injected with saline and placed in the black compartment for 45 min. On day 12, the control and METH‐Ext1 groups were injected with saline; PI and METH‐Ext2 groups were injected with psilocin, and all groups were placed in the white compartment for 45 min. On day 13, all mice were allowed to explore the two compartments freely for 15 min. This procedure was repeated three times over days 14–22.
In the reinstatement phase, four groups including Control, PI, METH‐Rein1 and METH‐Rein2 were tested. The METH‐Ext1 group was divided into METH‐Rein1 and METH‐Rein2 groups. The METH‐Rein1 group was injected (i.p) with METH, and the METH‐Rein2 group was injected (i.p) with 1 mg/kg psilocin prior to METH injections. The mice were then allowed to explore the two compartments freely for 15 min. At the end of the experimentation, the mice were sacrificed, and the PFC, NAc, and VTA were collected. Samples were stored at −80°C until subsequent use.
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EXT1 protein, human
EXT2 protein, human
Extinction, Psychological
Menstruation Disturbances
Metals
Methamphetamine
Mice, House
Pharmaceutical Preparations
psilocin
Saline Solution
SCH772984
Top products related to «SCH772984»
Sourced in United States, China, Germany, United Kingdom, Switzerland
SCH772984 is a chemical compound used in laboratory research. It functions as a small molecule inhibitor. The core purpose of this product is for use in scientific experimentation and analysis.
Sourced in United States, Germany, United Kingdom, France, China, Italy
Trametinib is a selective inhibitor of mitogen-activated protein kinase kinase (MEK) enzymes 1 and 2. It is a white to almost white crystalline powder that is used in various biomedical research applications.
Sourced in United States
SCH772984 is a laboratory reagent produced by MedChemExpress. It functions as an ATP-competitive inhibitor with selectivity for the ERK1/2 kinases. The product is intended for research use only.
Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal
Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
Sourced in United States, China, United Kingdom, Germany
MK-2206 is a selective allosteric Akt inhibitor that binds to the pleckstrin homology (PH) domain of Akt and inhibits its phosphorylation and activation. It has been used in research applications to study the role of Akt signaling in various cellular processes.
Sourced in United States, China, Germany, United Kingdom, Japan
LY294002 is a chemical compound used in research laboratories. It is a potent and selective inhibitor of the PI3 kinase enzyme.
Sourced in United States, Germany, France, China
Vemurafenib is a laboratory reagent used in research applications. It functions as a kinase inhibitor, specifically targeting the BRAF V600E mutation. This product is intended for research use only and its specific applications may vary depending on the research objectives.
Sourced in United States, China, United Kingdom, Germany, France, Australia, Canada, Japan, Italy, Switzerland, Belgium, Austria, Spain, Israel, New Zealand, Ireland, Denmark, India, Poland, Sweden, Argentina, Netherlands, Brazil, Macao, Singapore, Sao Tome and Principe, Cameroon, Hong Kong, Portugal, Morocco, Hungary, Finland, Puerto Rico, Holy See (Vatican City State), Gabon, Bulgaria, Norway, Jamaica
DMEM (Dulbecco's Modified Eagle's Medium) is a cell culture medium formulated to support the growth and maintenance of a variety of cell types, including mammalian cells. It provides essential nutrients, amino acids, vitamins, and other components necessary for cell proliferation and survival in an in vitro environment.
Sourced in United States
SCH772984 is a small molecule that functions as a selective and potent inhibitor of the enzyme LRRK2 (leucine-rich repeat kinase 2). It is a chemical compound used for research purposes.
Sourced in United States, Germany, China, United Kingdom, Canada
PD0325901 is a cell-permeable small molecule that selectively inhibits the mitogen-activated protein kinase (MAPK) pathway by targeting MEK1/2. It is commonly used in cell culture research applications.
More about "SCH772984"
Discover the power of SCH772984, a potent and selective inhibitor of the PI3K/mTOR signaling pathway.
This compound has been extensively studied for its potential therapeutic applications in various disease states, including cancer, neurological disorders, and metabolic conditions.
Dive deeper into the science behind SCH772984 and its role in regulating cell growth, proliferation, and survival.
Explore related compounds like Trametinib, MK-2206, LY294002, Vemurafenib, and PD0325901, and how they interact with the PI3K/mTOR pathway.
Optimize your SCH772984 research with the help of PubCompare.ai, the leading AI-driven platform.
Access protocols from literature, pre-prints, and patents, and leverage AI-driven comparisons to identify the best protocols and products.
Streamline your research with PubCompare.ai's powerful tools and expertise, and enhance the reproducibility and accuracy of your findings.
Whether you're working with SCH772984, FBS, DMEM, or any other related compounds, PubCompare.ai can help you navigate the complex world of biomedical research and unlock new insights.
Experience the power of AI-driven optimization and take your SCH772984 research to new heights.
This compound has been extensively studied for its potential therapeutic applications in various disease states, including cancer, neurological disorders, and metabolic conditions.
Dive deeper into the science behind SCH772984 and its role in regulating cell growth, proliferation, and survival.
Explore related compounds like Trametinib, MK-2206, LY294002, Vemurafenib, and PD0325901, and how they interact with the PI3K/mTOR pathway.
Optimize your SCH772984 research with the help of PubCompare.ai, the leading AI-driven platform.
Access protocols from literature, pre-prints, and patents, and leverage AI-driven comparisons to identify the best protocols and products.
Streamline your research with PubCompare.ai's powerful tools and expertise, and enhance the reproducibility and accuracy of your findings.
Whether you're working with SCH772984, FBS, DMEM, or any other related compounds, PubCompare.ai can help you navigate the complex world of biomedical research and unlock new insights.
Experience the power of AI-driven optimization and take your SCH772984 research to new heights.