MS5033
MS5033 is a CRBN-recruiting PROTAC degrader that targets AKT1. The IC50 values of MS5033 against human AKT range from 1.3 nM to 798 nM, with Kd values ranging from 4.8 nM to 160 nM. MS5033 inhibits downstream AKT signaling pathways, including the phosphorylation of PRAS40, thereby suppressing cancer cell proliferation and colony formation and inducing cancer cell apoptosis. MS5033 can be used in research on glioma, prostate cancer, triple-negative breast cancer, breast cancer and solid tumors.
(Pink: Akt ligand (HY-48682); Blue: Cereblon ligand (HY-10984); Black: linker (HY-133051)).
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2376137-29-8
- Formel: C51H66ClN11O11
- Molecular Weight:1044.59
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| PC-3 | DC50 |
430 nM
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Concentration-dependent AKT degradation in human PC3 prostate cancer cells assessed via immunoblotting, with maximum degradation observed after 24 h incubation at 1 μM.
Concentration-dependent AKT degradation in human PC3 prostate cancer cells assessed via immunoblotting, with maximum degradation observed after 24 h incubation at 1 μM.
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35119851 |
| PC-3 | GI50 |
10.8 μM
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Antiproliferative activity against human PC3 prostate cancer cells assessed as reduction in cell confluence monitored over 3-5 days by live cell imaging.
Antiproliferative activity against human PC3 prostate cancer cells assessed as reduction in cell confluence monitored over 3-5 days by live cell imaging.
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35119851 |
| MDA-MB-468 | GI50 |
4.8 μM
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Antiproliferative activity against human MDA-MB-468 triple-negative breast cancer cells assessed as reduction in cell confluence monitored over 3-5 days by live cell imaging.
Antiproliferative activity against human MDA-MB-468 triple-negative breast cancer cells assessed as reduction in cell confluence monitored over 3-5 days by live cell imaging.
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35119851 |
In Vitro
MS5033 (2 μM; 12 h) induces formation of the AKT-MS5033-CRBN ternary complex in E. coli-expressing HEK 293T cells, as measured by EGFP-based BiFC fluorescence[1].
MS5033 (2 μM; 12 h) induces formation of the AKT-MS5033-mutant CRBN ternary complex in mEAEC-expressing HEK 293T cells, as measured by EGFP-based BiFC fluorescence, without causing degradation of the reporter's AKT fusion protein[1].
MS5033 (2 μM; 24 h) induces degradation of the NLuc-AKT fusion protein in LALC-expressing HEK 293T cells, as measured by Western blotting, with residual protein levels at 0.45-fold of the DMSO control[1].
MS5033 (Compound 35) binds with high affinity to AKT1 and AKT3, and moderate affinity to AKT2 purified protein isoforms, with Kd values of 4.8 nM, 22 nM, and 160 nM, respectively[3].
MS5033 (Compound 62) inhibits purified AKT1, AKT2, and AKT3 kinases with IC50 values of 798 nM, 90 nM, and 544 nM, respectively[2].
MS5033 (30 nM-10 μM; 4-24 h) induces potent, time- and concentration-dependent, VHL- and ubiquitin-proteasome system-dependent AKT degradation in SW620 KRASG12C mutant colorectal cancer cells with a DC50 of 23 nM[2].
MS5033 (100 nM-1 μM) effectively induces AKT degradation in KRAS/BRAF mutant cancer cells (Colo205, HT-29, SKMEL 239, PANC-1) at 1 μM, with complete degradation in PANC-1 cells at 100 nM, and modest activity in Mia PaCa-2 cells[2].
MS5033 (1 μM; 18 h) acts as a selective AKT degrader in SW620 KRASG12D colorectal cancer cells, significantly reducing AKT1 and AKT2 protein levels with no substantial off-target degradation[2].
MS5033 effectively inhibits colony formation in PC3 PI3K/PTEN pathway mutant prostate cancer cells with potency comparable to related AKT PROTACs[2].
MS5033 (1-10 μM; 24 h) induces robust AKT degradation and downstream signaling inhibition in BT474 human breast cancer cells[3].
MS5033 (1 μM; 24 h) induces concentration-dependent AKT degradation in PC3 human prostate cancer cells with a DC50 of 430 nM, acting via a cereblon (CRBN)- and ubiquitin-proteasome system (UPS)-dependent mechanism, and reaches maximum degradation[3].
MS5033 (3-5 days) inhibits proliferation of PC3 human prostate cancer cells with a GI50 of 10.8 μM and MDA-MB-468 human triple-negative breast cancer cells with a GI50 of 4.8 μM[3].
MS5033 inhibits proliferation of SW620 KRASG12C mutant colorectal cancer cells with a GI50 of 3.1 μM, induces apoptosis, and suppresses colony formation, with activity dependent on AKT degradation[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HEK 293T cells stably expressing wild-type luciferase-based AKT-PROTAC-Reporter (LALC: NLuc-AKT-P2A-CLuc-CRBN)
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Concentration:2 μM
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Incubation Time:24 h
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Result:Reduced HA-LA (NLuc-AKT) protein levels to 0.45-fold of the DMSO control level, indicating degradation of the reporter's AKT fusion protein via the ubiquitin-proteasome pathway.
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Cell Line:SW620 KRAS mutant colorectal cancer cells
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Concentration:30 nM-10 μM (concentration-dependent AKT degradation); 1 μM (time-course analysis)
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Incubation Time:4 h, 12 h, 24 h (time-course analysis)
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Result:Induced potent, concentration-dependent total AKT degradation with a DC50 of 23 nM.
Achieved substantial total AKT depletion at 30 nM, near-complete degradation at 100 nM, with no hook effect observed up to 10 μM.
Induced significant AKT degradation at 4 h, near-complete degradation at 12 h, and sustained degradation for at least 24 h.
Rescued AKT degradation was observed with pretreatment of VHL-2, NEDD8-activating enzyme inhibitor, or proteasome inhibitor MG132.
Completely blocked AKT degradation was observed with pretreatment of AKT inhibitor ARQ-092.
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Cell Line:BT474 human breast cancer cells
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Concentration:1-10 μM
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Incubation Time:24 h
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Result:Reduced T-AKT protein levels significantly at 1 μM.
Inhibited phosphorylation of ribosomal protein S6 effectively.
Showed more potent activity than analogs with shorter PEG linkers, alkyl linkers, or modified CRBN binder moieties.
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Cell Line:PC3 human prostate cancer cells
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Concentration:1 μM; titration series (concentration-dependent degradation); pretreatments with 1 μM pomalidomide, 1 μM MLN4924, 20 μM MG-132, or 1 μM AZD5363
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Incubation Time:8 h, 24 h (time-course analysis)
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Result:Induced concentration-dependent total AKT degradation with a DC50 of 430 nM.
Achieved significant AKT downregulation at 8 h.
Reached maximum degradation at 24 h.
Diminished AKT-degrading activity was observed after pretreatment with pomalidomide, MLN4924, MG-132, or AZD5363.
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Cell Line:PC3 human prostate cancer cells, MDA-MB-468 human triple-negative breast cancer cells
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Concentration:titration series (GI50 measurement)
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Incubation Time:3-5 days
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Result:Inhibited PC3 cell growth with a GI50 of 10.8 μM.
Inhibited MDA-MB-468 cell growth with a GI50 of 4.8 μM.
Parmacokinetics
| Species | Dose | Route | Cmax | Tmax | AUC |
|---|---|---|---|---|---|
| Mice[3] | 150 mg/kg | i.p. | 8 μM | 1 h | 32500 ng·h/mL |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Swiss Albino (male, 6 weeks old)[3]
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Dosage:150 mg/kg
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Administration:i.p.; single dose
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Result:Achieved a maximum plasma concentration (Cₘₐₓ) of 8 μM at 1 h.
Reached an area under the curve (AUC) value of 32500 h·ng/mL.
Was well tolerated by mice with no reported toxicity.
Chemical Information
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CAS. Nr. 2376137-29-8
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Molecular Weight 1044.59
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Formel C51H66ClN11O11
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SMILES
O=C1C2=C(NCCOCCOCCOCCOCCOCCC(N3CCN(CC3)CC[C@@H](C4=CC=C(C=C4)Cl)NC(C5(CCN(C6=C7C(NC=C7)=NC=N6)CC5)N)=O)=O)C=CC=C2C(N1C8C(NC(CC8)=O)=O)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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Somatic Cell Culture
A method of simulating the in vivo environment in vitro to maintain the cell growth, differentation and main functions.
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CFSE Dye Dilution Proliferation Assay
The CFSE (carboxyfluorescein diacetate succinimidyl ester) dye dilution proliferation assay is based on the covalent labeling of intracellular proteins by a cell-permeant fluorescent dye that becomes fluorescent upon intracellular ester cleavage and then is stably retained within cells. As labeled cells divide, the dye is partitioned equally between daughter cells, resulting in a stepwise halving of fluorescence intensity that can be quantified by flow cytometry to determine the number of cell divisions undergone by each cell population. This fluorescence dilution approach enables quantitative tracking of lymphocyte proliferation at the single-cell level over multiple rounds of division. CFSE-based proliferation analysis has been widely applied to measure antigen-driven lymphocyte expansion in vitro, where discrete fluorescence peaks correspond to successive cell divisions and allow reconstruction of proliferative history within heterogeneous populations.
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Dye-dilution cell tracking and proliferation staining
Dye-dilution cell tracking assays quantify cell proliferation by covalently labeling intracellular proteins with a stable fluorescent dye that is equally partitioned between daughter cells during mitosis, resulting in stepwise halving of fluorescence intensity with each cell division as measured by flow cytometry histograms. Carboxyfluorescein diacetate succinimidyl ester (CFSE) is a prototypical dye that diffuses into cells, is enzymatically converted into a fluorescent compound, and then covalently binds intracellular amine groups, producing long-lived fluorescence suitable for tracking multiple rounds of division in vitro and in vivo. Successive generations of dividing cells form discrete peaks of decreasing fluorescence intensity, enabling estimation of proliferation history, precursor frequency, and division index within heterogeneous populations. Alternative dyes such as CellTrace Violet (CTV) and far-red membrane dyes (e. g. , PKH26) follow the same dilution principle but differ
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CCK-8/WST-8 Cell Proliferation Assay
The CCK-8/WST-8 assay is based on the reduction of the water-soluble tetrazolium salt WST-8 to a water-soluble formazan product by cellular dehydrogenases in metabolically active cells, where the generated formazan amount is proportional to the number of living cells and is quantified by measuring absorbance in the visible range, providing a colorimetric readout for cell viability and proliferation assessment. This class of tetrazolium-based assays improves upon earlier MTT-based systems by producing a water-soluble formazan, eliminating the need for organic solubilization steps and enabling direct spectrophotometric measurement in culture medium.
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Cell Counting-Based Growth Curve Assay
Cell counting-based growth curve assays quantify cell proliferation by directly measuring changes in viable cell number over time using manual or automated counting methods such as hemocytometer-based counting or instrument-assisted cell enumeration, enabling construction of growth curves that reflect population expansion dynamics in response to culture conditions. A widely used approach is trypan blue exclusion with hemocytometer counting, where membrane-compromised (non-viable) cells take up the dye, allowing discrimination between viable and non-viable cells while simultaneously enabling total cell number quantification. Repeated sampling across time points allows estimation of proliferation rate, growth phases, and comparative growth kinetics between experimental conditions.
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Colony Formation (Clonogenic) Assay
The clonogenic (colony formation) assay measures the ability of a single cell to retain reproductive viability and form a macroscopic colony, typically defined as a cluster derived from one progenitor cell after a defined growth period. This assay is widely used to evaluate cell survival after exposure to ionizing radiation or cytotoxic treatments and is considered a standard method in radiation biology for generating dose-response relationships of reproductive cell death. Colony formation reflects long-term proliferative capacity rather than short-term metabolic activity, and survival is quantified by comparing treated versus untreated conditions based on colony number and derived survival fractions.
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
The EdU incorporation assay measures DNA synthesis by adding the thymidine analog 5-ethynyl-2′-deoxyuridine to cells or tissues, where it is incorporated into newly synthesized DNA during S phase. Incorporated EdU is detected by copper-catalyzed azide-alkyne cycloaddition, in which a fluorescent azide covalently reacts with the ethynyl group on EdU, allowing S-phase cells to be detected by fluorescence microscopy, flow cytometry, or high-content imaging. EdU detection does not require DNA denaturation or anti-BrdU antibody access, which preserves sample structure and improves compatibility with immunostaining and multiparameter cytometry compared with BrdU-based detection. EdU can be cytotoxic in a cell-type- and exposure-dependent manner, so pulse duration, concentration, and continuous-labeling designs should be validated for each cell type.
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Ki-67 Immunostaining Proliferation Assay
Ki-67 immunostaining measures the growth fraction of a cell population by detecting Ki-67, a nuclear antigen present in proliferating cells and absent in quiescent G0 cells. The readout is the percentage of Ki-67-positive nuclei among total counted cells, commonly called the Ki-67 labeling index or proliferation index.
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Detection of Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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PCNA Immunodetection Proliferation Assay
PCNA immunodetection measures proliferative activity by detecting proliferating cell nuclear antigen, a nuclear protein associated with DNA polymerase δ function and DNA replication. The assay readout is the proportion of PCNA-positive nuclei among total counted cells, but PCNA labeling is not identical to BrdU labeling because PCNA can mark late G1/early S-associated replication competence and may persist beyond active DNA synthesis depending on fixation and extraction conditions.
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Protocol for Cell Counting and Cell Density Analysis
Cell counting and cell-density analysis estimate the number of cells in a known volume or field area. Manual hemocytometer counting uses a chamber of defined geometry to convert counted cells into cells/mL, while automated counters and image-analysis workflows detect cell objects from optical, brightfield, fluorescence, impedance, or digital-image features. Trypan blue viability counting is based on dye exclusion: viable cells with intact membranes exclude dye, while non-viable cells with compromised membranes stain blue. The readout is total cell density, viable-cell density, dead-cell density, and percent viability. Cell density can also be estimated from microscopy images by counting objects per image area, from flow cytometry using calibrated volume or reference particles, or from in situ microscopy in bioreactors after calibration against reference methods such as hemocytometer or flow cytometry.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
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Soft Agar Colony Formation Assay
Soft agar colony formation assay measures anchorage-independent growth, in which transformed or tumorigenic cells proliferate as colonies in a semisolid agar matrix while many non-transformed adherent cells fail to proliferate without attachment; classic studies showed that growth in semisolid medium correlates with tumorigenicity in nude mice, and later protocol papers describe the method as a stringent in vitro assay for malignant transformation. The readout is the number, size, morphology, or signal intensity of colonies formed within agar after incubation; published formats include manual colony counting after staining, 96-well or 384-well quantitative formats, DNA-binding dye detection, MTT/tetrazolium-based detection, digital image analysis, and PCR-based marker detection from soft agar cultures.
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MTT Cell Proliferation Assay
The MTT assay is a colorimetric endpoint assay for estimating viable cell number, cell growth, cytotoxicity, or cell activation in cultured mammalian cells. Living cells reduce the yellow tetrazolium salt MTT into purple/blue formazan, while dead cells do not generate the same signal; the resulting color can be quantified with a multiwell spectrophotometer. MTT reduction is commonly interpreted as a readout of metabolic activity that often correlates with viable cell number, but it should not be treated as a direct cell-counting method unless the assay is optimized for the cell type and experimental condition. Studies show that MTT reduction can involve mitochondrial and non-mitochondrial reducing systems, and formazan may accumulate in intracellular lipid droplets rather than simply marking mitochondria.
Reinheit & Dokumentation
Verweise
[2]. Yu X, et al. Novel Allosteric Inhibitor-Derived AKT Proteolysis Targeting Chimeras (PROTACs) Enable Potent and Selective AKT Degradation in KRAS/BRAF Mutant Cells. Journal of medicinal chemistry. 2022 Oct 27;65(20):14237-14260. [Content Brief]
[3]. Yu X, et al. Discovery of Potent, Selective, and In Vivo Efficacious AKT Kinase Protein Degraders via Structure-Activity Relationship Studies. Journal of medicinal chemistry. 2022 Feb 24;65(4):3644-3666. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)