Trametinib

Manufactured by Selleck Chemicals

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.

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Lab products found in correlation

439 protocols using trametinib

Establishing Trametinib-Resistant Cell Lines

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The HSC3 and CAL27 trametinib-resistant (HSC3-TR, CAL27-TR) lines were generated by culturing HSC3 and CAL27 parental lines with sequentially increasing concentrations of trametinib (Selleckchem) up to 1 µM trametinib. Simultaneously, HSC3 and CAL27 parental cells were cultured in media containing DMSO (0.01%, Sigma Aldrich) to generate control lines (HSC3-C and CAL27-C).

Mudianto T., Campbell K.M., Webb J., Zolkind P., Skidmore Z.L., Riley R., Barnell E.K., Ozgenc I., Giri T., Dunn G.P., Adkins D.R., Griffith M., Egloff A.M., Griffith O.L, & Uppaluri R. (2021). Yap1 Mediates Trametinib Resistance in Head and Neck Squamous Cell Carcinomas. Clinical cancer research : an official journal of the American Association for Cancer Research.

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Pharmacological Modulation of Signaling Pathways

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For in vitro studies: PGF2α (Cayman), rmFGF1 (Peprotech), rmPDGFBB (Peprotech), rmPDGFAA (Peprotech), rh/mWnt-5a (R&D), LPA (Santa Cruz biotech), rmIL6 (Peprotech), S1P (Cayman), Adapalene (Selleckchem), SAG (Tocris), rmTGFβ1(R&D), rmTGFβ2(R&D), rmTGFβ3 (R&D), CCL2 (BioLegend), CCR2 inhibitor (Santa Cruz Biotechnology), MEKi (PD0324901, 2 μM, Selleckchem), PI3Ki (LY294002, 2 μM, Selleckchem) , mTORi (Rapamycin, 100 nM, Selleckchem), Trametinib (Selleckchem, 50 nM), Alpelisib (Selleckchem, 5 μM) and ARS-1620 (MedChemExpress).
For in vivo studies: TGFβ neutralizing antibody (BioXCell, Clone 1D11, 200 μg, every other day, i.p), Clodronate liposome (Liposoma, 0.1 ml per 10 mg weight, every 5 days, i.p), Trametinib (Selleckchem, 0.3 or 1 or 3 mg/kg as indicated, q.d., oral), Alpelisib (Selleckchem, 50 mg/kg, once per day, oral), ARS-1620 (MedChemExpress, 200 mg/kg, q.d., oral), LMK-235 (MedChemExpress, 5 mg/kg, q.d., i.p.), Galunisertib (Selleckchem, 50 mg/kg, b.i.d., oral), mouse CCL2 neutralizing antibody (BioXCell, 5 mg/kg, every 2 days, i.p.), and RS 504393 (Cayman, 2 mg/kg, q.d., i.p.).

Hou P., Kapoor A., Zhang Q., Li J., Wu C.J., Li J., Lan Z., Tang M., Ma X., Ackroyd J.J., Kalluri R., Zhang J., Jiang S., Spring D.J., Wang Y.A, & DePinho R.A. (2020). Tumor microenvironment remodeling enables bypass of oncogenic KRAS dependency in pancreatic cancer. Cancer discovery, 10(7), 1058-1077.

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Modulation of Glioblastoma Sphere Radiosensitivity

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The GB-derived spheres were treated according to previously published protocols [26 (link),32 (link)]. Briefly, the following conditions were applied: (1) 1 µM of the HDACi MS-275 (S1053; purchased from Selleck Chemicals), (2) 1 µM of the MEKi TAK-733 (S2617; purchased from Selleck Chemicals), (3) 1 µM trametinib (S2673; purchased from Selleck Chemicals), (4) a combination of 1 µM MS-275 plus 1 µM TAK-733 or (5) a combination of 1 µM MS-275 plus 1 µM trametinib. Where specified, the GB-derived spheres were treated with the standard compound TMZ at 50 µM (SC-203292; purchased from Santa Cruz Biotechnology, Dallas, TX, USA) for comparison. All compounds were diluted to give a final concentration of 1% v/v DMSO and the controls were treated with 1% v/v DMSO. The GB-derived spheres were treated 72 h after seeding the cells to allow time for sphere formation. After 24 h of compound treatment, the spheres were irradiated at room temperature with X-rays using an X-Strahl RS225 radiation device (X-Strahl LTD, Camberlay, UK). The 4 Gy irradiation dose was delivered at a rate of 0.824 Gy/min using a 3 mm aluminum filter. The sham irradiated controls were handled under the same conditions but were not exposed to radiation.

Essien E.I., Hofer T.P., Atkinson M.J, & Anastasov N. (2022). Combining HDAC and MEK Inhibitors with Radiation against Glioblastoma-Derived Spheres. Cells, 11(5), 775.

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Clonal Analysis of Hematopoietic Cells

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One million peripheral blood (PB) or 2 × 10⁵ BM cells were seeded in methylcellulose-based medium Methocult H4034 (StemCell Technologies, Meda, Italy), according to manufacturer's instructions, and plated in 6-well dishes. After 2 weeks of incubation at 37°C, 5% CO₂, individual colonies were picked, washed in PBS, and lysed in 20 μL of the following buffer: 10 mM Tris-HCl, 50 mM NaCl, 6.25 mM MgCl₂, 0.045% NP40, 0.45% Tween-20; pH 7.6. On average 50 colonies per sample were isolated. After adding 1 μL of 20 μg/mL proteinase K, the lysate was incubated at 56°C for 1 hour and at 95°C for 15 minutes. Subsequently, the sample was amplified using dedicated barcoded primers by PCR, and underwent deep-sequencing. For combined treatment, 2 × 10⁵ BM-derived cells were seeded in methylcellulose-based medium in presence of phosphoethanolamine 1 mM (Merck Life Science, Milan, Italy), trametinib 10 nM (Selleck Chemicals, Rome, Italy), trametinib 100 nM and combination of them. After 2 weeks of incubation, colonies were counted. Expected additive effect of the combination viability is the product of the 2 singlet viabilities. For actionable mutations targeting, all the inhibitors used (crizotinib, dasatinib, imatinib, and ruxolitinib) were purchased from Selleck Chemicals.

Fontana D., Ramazzotti D., Aroldi A., Redaelli S., Magistroni V., Pirola A., Niro A., Massimino L., Mastini C., Brambilla V., Bombelli S., Bungaro S., Morotti A., Rea D., Stagno F., Martino B., Campiotti L., Caocci G., Usala E., Merli M., Onida F., Bregni M., Elli E.M., Fumagalli M., Ciceri F., Perego R.A., Pagni F., Mologni L., Piazza R, & Gambacorti-Passerini C. (2020). Integrated Genomic, Functional, and Prognostic Characterization of Atypical Chronic Myeloid Leukemia. HemaSphere, 4(6), e497.

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Xenograft Mouse Model for SCID Tumor Study

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Approximately 6–8 week-old female SCID mice (NOD.CB17-Prkdc;
Envigo RMS.Inc) were injected subcutaneously with 5 × 10⁶CAL62 or CAL62-splice cells grown to 70% confluence and resuspended in 50%
Matrigel (CORNING) into the right and left flanks, respectively. Treatments were
administered by oral gavage when tumor volume approached 200 mm³ as
estimated by measuring the length and width with calipers (width²× length × 0.52). Tumor-bearing mice were randomly assigned into 5
treatment arms: Controls (vehicle-4% DMSO in 30% PEG 300); AZD8055 (10 mg/kg);
Trametinib (0.75 mg/kg); JQ1 (40 mg/kg); AZD8055 + Trametinib and AZD8055 + JQ1
(all drugs were from Selleckchem). Mice were weighed at the start of treatment
and every second day during the treatment period. AZD8055 was dissolved in a
mixture of 4% DMSO and 30% PEG 300 (SIGMA), Trametinib in 4% DMSO in corn oil
and JQ1 in 2% DMSO, 30% PEG 300 and 5% Tween 80. Treatments were administered by
oral gavage in a volume of approximately 200 μL. Tumor volume was
measured every 2–3 days with calipers. After 21 days mice were humanely
killed, and dissected tumors flash frozen for subsequent protein isolation. All
animal experiments were performed in accordance with a protocol approved by the
Institutional Animal Care and Use of Committee (IACUC) of Memorial Sloan
Kettering Cancer Center.

Krishnamoorthy G.P., Davidson N.R., Leach S.D., Zhao Z., Lowe S.W., Lee G., Landa I., Nagarajah J., Saqcena M., Singh K., Wendel H.G., Dogan S., Tamarapu P.P., Blenis J., Ghossein R.A., Knauf J.A., Rätsch G, & Fagin J.A. (2018). EIF1AX and RAS mutations cooperate to drive thyroid tumorigenesis through ATF4 and c-MYC. Cancer discovery, 9(2), 264-281.

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Melanoma Cell Lines Pharmacological Treatment

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The human melanoma cell lines used—A375, SK-MEL-190,
WM266–4, SK-MEL-100, SK-MEL-5, and Mel537—have been extensively
characterized (37 (link)). Cells are routinely
tested for mycoplasma contamination by DAPI staining and passaged no more than
one month prior to experiments. Cells were cultured in DMEM (A375,
WM266–4) or RPMI (SK-MEL-190, SK-MEL-100, SK-MEL-5, and Mel537)
supplemented with 10% fetal bovine serum and 1% penicillin-streptomycin.
Dabrafenib and trametinib were purchased from Selleck and dissolved in DMSO.
Cultures were treated with DMSO as control or with 100nM Dabrafenib and 10nM
trametinib in combination for 48 trametinib.

Brighton H.E., Angus S.P., Bo T., Roques J., Tagliatela A.C., Darr D.B., Karagoz K., Sciaky N., Gatza M.L., Sharpless N.E., Johnson G.L, & Bear J.E. (2017). New mechanisms of resistance to MEK inhibitors in melanoma revealed by intravital imaging. Cancer research, 78(2), 542-557.

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Xenograft Mouse Model for Cancer Research

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All animal experiments were performed in accordance with E.U. directive 2010/63 (regional Gothenburg animal ethics committee approval #287/289–12 and #36–2014). For cell line xenografts, cells were suspended in RPMI, mixed 1:1 with Matrigel (BD Biosciences), and 2 × 10⁵ cells transplanted subcutaneously into the flanks of immunocompromised, non-obese severe combined immune deficient interleukin-2 chain receptor γ knockout mice (NOG mice; Taconic, Denmark). For transcriptome analyses, all CDX tumors were harvested once they reached 100 −200 mm³ in size. To assess effects of trametinib, xenografts whose growth were increased on two consecutive measurements, were randomized to two treatment groups: vehicle or trametinib (4 mg compound/kg food = 1 mg/kg/day) (Selleckchem, Houston, TX) mixed in the fodder (ResearchDiets Inc., New Brunswick, NJ). Mice were weighed and tumors measured using calipers twice a week. Mice were euthanized when tumors were larger than 10 × 10 mm² as per ethical regulations [55 (link)].

Bhadury J., Einarsdottir B.O., Podraza A., Bagge R.O., Stierner U., Ny L., López M.D, & Nilsson J.A. (2016). Hypoxia-regulated gene expression explains differences between melanoma cell line-derived xenografts and patient-derived xenografts. Oncotarget, 7(17), 23801-23811.

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Melanoma Cell Lines and Kinase Inhibitors

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Human melanoma cell line M230 was provided by Pr A. Ribas and was cultured in RPMI 1640 (Invitrogen, Cergy Pontoise, France) containing 10% (v/v) fetal calf serum (FCS; Perbio, Bredières, France), L-glutamin (2 mM; Gibco, Cergy pontoise, France), antibiotics (100 U/mL penicillin and 1000 μg/mL streptomycin; Gibco). Human melanoma cell lines HBL and LND1 were provided by Pr G E Gahnem and were cultured in F10 (Invitrogen) containing 10% (v/v) fetal calf serum (FCS; Perbio), L-glutamin (2 mM; Gibco), antibiotics (100 U/mL penicillin and 1000 μg/mL streptomycin; Gibco). Imatinib, nilotinib, sorafenib, dasatinib, pexidartinib, and trametinib were from Selleck Chemicals, dissolved in DMSO and used at 1 µM final concentration for KIT inhibitors and 0.2 µM for trametinib. FGF2 was from PeproTech and used at 20 ng/mL final concentration.

Tétu P., Delyon J., André J., Reger de Moura C., Sabbah M., Ghanem G.E., Battistella M., Mourah S., Lebbé C, & Dumaz N. (2020). FGF2 Induces Resistance to Nilotinib through MAPK Pathway Activation in KIT Mutated Melanoma. Cancers, 12(5), 1062.

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Trametinib-Resistant MOLM13 Cell Model

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Human MOLM13 cells with FLT3-ITD mutation, were obtained from the Sanger Institute Cancer Cell Line Panel. Cell lines were maintained in RPMI 1640 (Gibco) supplemented with 20% Fetal Bovine Serum (HyClone), 2% L-glutamine, 1% penicillin/streptomycin (Life Technologies).Trametinib-resistant MOLM13 cell lines were generated by culturing MOLM13 cells in increasing concentrations of Trametinib (Selleck).
Cell viability was measured bi-weekly and cells were replenished with new media and Trametinib.
Resistance was assessed using the MTS assay for drug sensitivity. Once resistant, cell lines were maintained in 50nM Trametinib added bi-weekly. Cell lines were screened for mycoplasma contamination on a monthly schedule.
For proteomic and phosphorproteomic pro ling, 5 million parental MOLM13 (N=3) and resistant MOLM13 (N=3) cell lines were starved overnight in starvation media (RPMI supplemented with 0.1% BSA). Trametinib (50nM) was added to the starvation media of the resistant cell lines. Cells were washed three times in PBS, pelleted and ash frozen.

Gosline S.J., Tognon C.E., Nestor M., Joshi S.K., Modak R.V., Damnernsawad A., Posso C., Moon J., Hansen J., Hutchinson C., Pino J.C., Gritsenko M., Weitz K., Traer E., Tyner J.W., Druker B.J., Agarwal A., Piehowski P., McDermott J., & Rodland K. (2022). Proteomics and Phosphoprotoemic Measurements Enhance Ability to Predict Ex Vivo Drug Response in AML.

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Cell Viability Assay of Anti-Cancer Drugs

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The effect of PD0325901, trametinib, perifosine (SelleckChem, Houston, TX, USA) or DMF (FUJIFILM Wako) on cell viability was examined using the trypan blue stain exclusion assay as previously described [37 (link),51 (link)]. DLD-1, HT-29, LoVo, Colo-205, LoVo/PR, Colo-205/PR and LoVo/TR cells were seeded onto flat-bottom 96-well plates for 24 h. Next, DLD-1, HT-29, LoVo and Colo-205 cells were treated with various concentrations of PD0325901 or trametinib for 1, 3 or 5 days; combination treatment with PD0325901 or trametinib and perifosine or DMF for 3 days; and LoVo/PR, LoVo/TR and Colo-205/PR cells were treated with various concentrations of PD0325901 or trametinib with or without perifosine for 3 days. A 0.4% trypan blue solution was mixed with the cell cultures and loaded into a hemocytometer. The cell survival rate represented the survival ((unstained cells)/death (stained cells)) rate on each day.

Tsubaki M., Takeda T., Noguchi M., Jinushi M., Seki S., Morii Y., Shimomura K., Imano M., Satou T, & Nishida S. (2019). Overactivation of Akt Contributes to MEK Inhibitor Primary and Acquired Resistance in Colorectal Cancer Cells. Cancers, 11(12), 1866.

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