EOS Med Chem produce Evofosfamide,TH 302, 918633-87-1 in GMP plant, C-GMP standard, now COA, NMR, HPLC, MS is ok

Name: Evofosfamide

CAS#: 918633-87-1

Chemical Formula: C9H16Br2N5O4P

Exact Mass: 446.93067

Molecular Weight: 449.04

Elemental Analysis: C, 24.07; H, 3.59; Br, 35.59; N, 15.60; O, 14.25; P, 6.90

Description: Evofosfamide, also known as TH-302, is a hypoxia-activated prodrug consisting of a 2-nitroimidazole phosphoramidate conjugate with potential antineoplastic activity. The 2-nitroimidazole moiety of hypoxia-activated prodrug TH-302 acts as a hypoxic trigger, releasing the DNA-alkylating dibromo isophosphoramide mustard moiety within hypoxic regions of tumors. Normoxic tissues may be spared due to the hypoxia-specific activity of this agent, potentially reducing systemic toxicity. Check for active clinical trials or closed clinical trials using this agent. (NCI).

Synonym: TH302; TH 302; TH-302. Evofosfamide

IUPAC/Chemical Name: Phosphorodiamidic acid, N,N'-bis(2-bromoethyl)-, (1-methyl-2-nitro-1H-imidazol-5-yl)methyl ester.

SMILES Code: O=P(NCCBr)(NCCBr)OCC1=CN=C([N+]([O-])=O)N1C

EOS Med Chem produce Evofosfamide,TH 302, 918633-87-1 in GMP plant, C-GMP standard, now COA, NMR, HPLC, MS is ok.

Evofosfamide,TH 302, 918633-87-1 Intermediates, EOS Med Chem have 8; Evofosfamide,TH 302, 918633-87-1 Impurity we have 10, all from GMP, FDA plant.

Now Evofosfamide,TH 302, 918633-87-1 DMF document is preparing.

Until 2016, Aug, Evofosfamide,TH 302, 918633-87-1 more than produced 25kg API, 120kg Intermediates

GMP PRODUCE:

Alectinib;Veliparib;Acalabrutinib;Venetoclax;Sotagliflozin;Ledipasvir;LX1606;Anacetrapib;Abemaciclib 

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2016 Korea(한국) CPHI, C40, Welcome!

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執大象，天下往，往而無害，安平泰

網址: www.eosmedchem.com 

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Evofosfamide TH-302;HAP-302 918633-87-1

Evofosfamide Intermediates (1-methyl-2-nitro-1H-imidazol-5-yl)methanol 39070-14-9

Evofosfamide Intermediates N,N'-Bis(2-bromoethyl)phosphorodiamidic acid 141025-16-3

According to wikipedia.com, TH-302 is an experimental anticancer agent that is in clinical development at Threshold Pharmaceuticals, Inc. It is activated only at very low levels of oxygen (hypoxia). Such levels are common in human solid tumors, a phenomenon known as tumor hypoxia. TH-302 exploits the activation of a nitroazole prodrug by a process that involves a one electron reduction mediated by ubiquitous cellular reductases such as the NADPH cytochrome P450 to generate a radical anion prodrug (RP). In the presence of oxygen (normoxia) the radical anion prodrug reacts rapidly with oxygen to generate the original prodrug and superoxide (SO). Under the low oxygen conditions of the hypoxic zones in tumors, however, the radical anion prodrug undergoes further irreversible reductions to the hydroxylamine (HA) followed by elimination, releasing the active drug and an azole derivative (AZ).

  

TH-302 started a Phase 1 clinical trial in 2007 in various solid tumors. The Phase 1 trial is a multi-center, open-label, dose-escalation study in patients with solid tumor cancers. The primary objectives of the study are to determine the maximum tolerated dose (MTD) and dose-limiting toxicities of TH-302 in patients with advanced solid tumors and to establish the appropriate dose to be tested in Phase 2 clinical trials. The secondary objectives of the trial include establishing the pharmacokinetics and assessing the anti-tumor activity of TH-302, as measured by objective response rate and duration of response, and to characterize the safety profile. Tumors will be evaluated at baseline and every eight weeks using the Response Evaluation Criteria In Solid Tumors (RECIST) criteria. 

EOS Med Chem produce BI-847325,1207293-36-4 in GMP plant, C-GMP standard, now COA, NMR, HPLC, MS is ok

Name: BI-847325

CAS#: 1207293-36-4

Chemical Formula: C29H28N4O2

Exact Mass: 464.2212

Molecular Weight: 464.569

Elemental Analysis: C, 74.98; H, 6.08; N, 12.06; O, 6.89

EOS Med Chem produce BI-847325,1207293-36-4 in GMP plant, C-GMP standard, now COA, NMR, HPLC, MS is ok.

BI-847325,1207293-36-4 Intermediates, EOS Med Chem have 8; BI-847325,1207293-36-4 Impurity we have 10, all from GMP, FDA plant.

Now BI-847325,1207293-36-4 DMF document is preparing.

Until 2016, Aug, BI-847325,1207293-36-4 more than produced 25kg API, 120kg Intermediates

GMP PRODUCE:

Alectinib;Veliparib;Acalabrutinib;Venetoclax;Sotagliflozin;Ledipasvir;LX1606;Anacetrapib;Abemaciclib 

2016 Mumbai CPHI, Hope to meet!

2016 Barcelona CPHI, Hope to meet!

2016 Korea(한국) CPHI, C40, Welcome!

2016 Shanghai CPHI, W5C47, Welcome!

EOS Med Chem, Medchem is Big

執大象，天下往，往而無害，安平泰

網址: www.eosmedchem.com 

郵箱: gutian@eosmedchem.com; eosmedchem@gmail.com 

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BI-847325 BI-847325 1207293-36-4

BI-847325 Intermediates N-ethylpropiolamide 2682-33-9

BI-847325 Intermediates 6-iodoindolin-2-one 919103-45-0

BI-847325 Intermediates (E)-3-(hydroxy(phenyl)methylene)-6-iodoindolin-2-one 1535204-23-9

BI-847325 Intermediates (E)-6-iodo-3-(phenyl((trimethylsilyl)oxy)methylene)-2-((trimethylsilyl)oxy)-3H-indole

BI-847325 Intermediates (Z)-3-(((4-((dimethylamino)methyl)phenyl)amino)(phenyl)methylene)-6-iodoindolin-2-one 1537909-08-2

Description: BI-847325 is an orally available dual inhibitor of mitogen-activated protein kinase kinase (MEK) and Aurora kinases, with potential antineoplastic activity. Upon oral administration, MEK/Aurora kinase inhibitor BI 847325 selectively binds to and inhibits the activity of MEK, which both prevents the activation of MEK-dependent effector proteins and inhibits growth factor-mediated cell signaling. BI 847325 also binds to and inhibits the activity of the Aurora kinases A, B and C which may disrupt the assembly of the mitotic spindle apparatus, prevent chromosome segregation, and inhibit both cellular division and proliferation in Aurora kinase-overexpressing tumor cells.

Synonym: BI-847325; BI 847325; BI847325.

IUPAC/Chemical Name: (Z)-3-(3-((4-((dimethylamino)methyl)phenylamino)(phenyl)methylene)-2-oxoindolin-6-yl)-N-ethylpropiolamide

SMILES Code: O=C(NCC)C#CC1=CC(NC/2=O)=C(C=C1)C2=C(NC3=CC=C(CN(C)C)C=C3)/C4=CC=CC=C4

1: Schöffski P, Aftimos P, Dumez H, Deleporte A, De Block K, Costermans J,

Billiet M, Meeus MA, Lee C, Schnell D, Goeldner RG, Awada A. A phase I study of

two dosing schedules of oral BI 847325 in patients with advanced solid tumors.

Cancer Chemother Pharmacol. 2016 Jan;77(1):99-108. doi:

10.1007/s00280-015-2914-5. Epub 2015 Dec 9. PubMed PMID: 26650227.

2: Phadke MS, Sini P, Smalley KS. The Novel ATP-Competitive MEK/Aurora Kinase

Inhibitor BI-847325 Overcomes Acquired BRAF Inhibitor Resistance through

Suppression of Mcl-1 and MEK Expression. Mol Cancer Ther. 2015 Jun;14(6):1354-64.

doi: 10.1158/1535-7163.MCT-14-0832. Epub 2015 Apr 14. PubMed PMID: 25873592;

PubMed Central PMCID: PMC4458462.

EOS Med Chem produce Refametinib,RDEA-119,BAY 869766, 923032-37-5 in GMP plant, C-GMP standard, now COA, NMR, HPLC, MS is ok.

Name: Refametinib

CAS#: 923032-37-5

Chemical Formula: C19H20F3IN2O5S

Exact Mass: 572.00897

Molecular Weight: 572.34

Elemental Analysis: C, 39.87; H, 3.52; F, 9.96; I, 22.17; N, 4.89; O, 13.98; S, 5.60

EOS Med Chem produce Refametinib,RDEA-119,BAY 869766, 923032-37-5 in GMP plant, C-GMP standard, now COA, NMR, HPLC, MS is ok.

Refametinib,RDEA-119,BAY 869766, 923032-37-5 Intermediates, EOS Med Chem have 8; Refametinib,RDEA-119,BAY 869766, 923032-37-5 Impurity we have 10, all from GMP, FDA plant.

Now Refametinib,RDEA-119,BAY 869766, 923032-37-5 DMF document is preparing.

Until 2016, Aug, Refametinib,RDEA-119,BAY 869766, 923032-37-5 more than produced 25kg API, 120kg Intermediates

GMP PRODUCE:

Alectinib;Veliparib;Acalabrutinib;Venetoclax;Sotagliflozin;Ledipasvir;LX1606;Anacetrapib;Abemaciclib 

2016 Mumbai CPHI, Hope to meet!

2016 Barcelona CPHI, Hope to meet!

2016 Korea(한국) CPHI, C40, Welcome!

2016 Shanghai CPHI, W5C47, Welcome!

EOS Med Chem, Medchem is Big

執大象，天下往，往而無害，安平泰

網址: www.eosmedchem.com 

郵箱: gutian@eosmedchem.com; eosmedchem@gmail.com 

辦公室: 0086-531-69905422-806(直通)

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Refametinib BAY-86-9766; AY-869766; RDEA-119; AR-119 923032-37-5

Refametinib Intermediates (S)-tert-butyldimethyl(oxiran-2-ylmethoxy)silane 123237-62-7

Refametinib Intermediates Butyl cyclopropanesulfonate 83635-12-5

Refametinib Intermediates (S)-butyl 1-(3-((tert-butyldimethylsilyl)oxy)-2-hydroxypropyl)cyclopropane-1-sulfonate 1335100-23-6

Refametinib Intermediates (S)-butyl 1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonate 1335100-30-5

Refametinib Intermediates (S)-butyl 1-((2,2-dimethyl-1,3-dioxolan-4-yl)methyl)cyclopropane-1-sulfonate 1335100-31-6

Refametinib Intermediates Sodium (S)-1-((2,2-dimethyl-1,3-dioxolan-4-yl)methyl)cyclopropane-1-sulfonate 1262760-34-8

Refametinib Intermediates (S)-1-((2,2-dimethyl-1,3-dioxolan-4-yl)methyl)cyclopropane-1-sulfonyl chloride 1262760-00-8

Refametinib Intermediates 2,3,5-trifluoro-N-(3-fluoro-4-iodophenyl)-6-nitroaniline 765962-71-8

Refametinib Intermediates 2,3-difluoro-N-(2-fluoro-4-iodophenyl)-5-methoxy-6-nitroaniline 923032-72-8

Refametinib Intermediates 5,6-difluoro-N1-(2-fluoro-4-iodophenyl)-3-methoxybenzene-1,2-diamine 923032-74-0

Refametinib Intermediates (S)-N-(3,4-difluoro-2-((2-fluoro-4-iodophenyl)amino)-6-methoxyphenyl)-1-((2,2-dimethyl-1,3-dioxolan-4-yl)methyl)cyclopropane-1-sulfonamide 1262760-18-8

Description: Refametinib, also known as RDEA119, BAY 86-9766, is an orally bioavailable selective MEK inhibitor with potential antineoplastic activity. MEK inhibitor RDEA119 specifically inhibits mitogen-activated protein kinase kinase 1 (MAP2K1 or MAPK/ERK kinase 1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a dual specificity threonine/tyrosine kinase, is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.

Synonym: RDEA119; RDEA-119; RDEA 119; BAY 869766; BAY-69766; BAY869766; BAY 86 9766; BAY 86-9766; BAY86-9766; BAY 869766

IUPAC/Chemical Name: (S)-N-(3,4-difluoro-2-((2-fluoro-4-iodophenyl)amino)-6-methoxyphenyl)-1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonamide

SMILES Code: O=S(C1(C[C@H](O)CO)CC1)(NC2=C(OC)C=C(F)C(F)=C2NC3=CC=C(I)C=C3F)=O

BAY 86-9766, formerly known as RDEA119, is currently being developed by Ardea. BAY 86-9766  is a potent, non-ATP competitive, highly-selective inhibitor of MEK. According to Ardea Inc's website, preclinical and clinical data suggest that BAY 86-9766 has favorable properties, including once-daily, oral dosing, excellent selectivity and limited retention in the brain, which may result in a reduced risk of central nervous system (CNS) side effects at doses expected to be effective, a problem associated with other members of this class of compounds. In addition, BAY 86-9766 has been shown to suppress tumor cell growth in-vitro and in-vivo. Phase 1 data have demonstrated that BAY 86-9766 has a long half-life and favorable pharmacokinetic properties, allowing for once-daily oral dosing. Preclinical in vitro and in vivo oncology studies have demonstrated significant potential synergy across multiple tumor types when BAY 86-9766 is used in combination with other approved anti-cancer therapeutics, including sorafenib (Nexavar®; Bayer HealthCare, Onyx Pharmaceuticals). (source: http://www.ardeabio.com/development-pipeline/cancer.htm ).

1: Wylie-Sears J, Levine RA, Bischoff J. Losartan inhibits endothelial-to-mesenchymal transformation in mitral valve endothelial cells by blocking transforming growth factor-β-induced phosphorylation of ERK. Biochem Biophys Res Commun. 2014 Mar 12. pii: S0006-291X(14)00445-8. doi: 10.1016/j.bbrc.2014.03.014. [Epub ahead of print] PubMed PMID: 24632204.

2: Weekes CD, Von Hoff DD, Adjei AA, Leffingwell DP, Eckhardt SG, Gore L, Lewis KD, Weiss GJ, Ramanathan RK, Dy GK, Ma WW, Sheedy B, Iverson C, Miner JN, Shen Z, Yeh LT, Dubowy RL, Jeffers M, Rajagopalan P, Clendeninn NJ. Multicenter phase I trial of the mitogen-activated protein kinase 1/2 inhibitor BAY 86-9766 in patients with advanced cancer. Clin Cancer Res. 2013 Mar 1;19(5):1232-43. doi: 10.1158/1078-0432.CCR-12-3529. Epub 2013 Feb 22. PubMed PMID: 23434733.

3: Gorges TM, Schiller J, Schmitz A, Schuetzmann D, Schatz C, Zollner TM, Krahn T, von Ahsen O. Cancer therapy monitoring in xenografts by quantitative analysis of circulating tumor DNA. Biomarkers. 2012 Sep;17(6):498-506. doi: 10.3109/1354750X.2012.689133. Epub 2012 May 23. PubMed PMID: 22616911.

4: Liu Z, Xing M. Induction of sodium/iodide symporter (NIS) expression and radioiodine uptake in non-thyroid cancer cells. PLoS One. 2012;7(2):e31729. doi: 10.1371/journal.pone.0031729. Epub 2012 Feb 16. PubMed PMID: 22359623; PubMed Central PMCID: PMC3281006.

5: Holm TM, Habashi JP, Doyle JJ, Bedja D, Chen Y, van Erp C, Lindsay ME, Kim D, Schoenhoff F, Cohn RD, Loeys BL, Thomas CJ, Patnaik S, Marugan JJ, Judge DP, Dietz HC. Noncanonical TGFβ signaling contributes to aortic aneurysm progression in Marfan syndrome mice. Science. 2011 Apr 15;332(6027):358-61. doi: 10.1126/science.1192149. PubMed PMID: 21493862; PubMed Central PMCID: PMC3111087.

6: Diep CH, Munoz RM, Choudhary A, Von Hoff DD, Han H. Synergistic effect between erlotinib and MEK inhibitors in KRAS wild-type human pancreatic cancer cells. Clin Cancer Res. 2011 May 1;17(9):2744-56. doi: 10.1158/1078-0432.CCR-10-2214. Epub 2011 Mar 8. PubMed PMID: 21385921; PubMed Central PMCID: PMC3265169.

7: Liu D, Xing J, Trink B, Xing M. BRAF mutation-selective inhibition of thyroid cancer cells by the novel MEK inhibitor RDEA119 and genetic-potentiated synergism with the mTOR inhibitor temsirolimus. Int J Cancer. 2010 Dec 15;127(12):2965-73. doi: 10.1002/ijc.25304. PubMed PMID: 21351275; PubMed Central PMCID: PMC2916062.

8: Chang Q, Chapman MS, Miner JN, Hedley DW. Antitumour activity of a potent MEK inhibitor RDEA119/BAY 869766 combined with rapamycin in human orthotopic primary pancreatic cancer xenografts. BMC Cancer. 2010 Sep 28;10:515. doi: 10.1186/1471-2407-10-515. PubMed PMID: 20920162; PubMed Central PMCID: PMC2955043.

9: Hou P, Bojdani E, Xing M. Induction of thyroid gene expression and radioiodine uptake in thyroid cancer cells by targeting major signaling pathways. J Clin Endocrinol Metab. 2010 Feb;95(2):820-8. doi: 10.1210/jc.2009-1888. Epub 2009 Dec 11. PubMed PMID: 20008023; PubMed Central PMCID: PMC2840852.

10: Iverson C, Larson G, Lai C, Yeh LT, Dadson C, Weingarten P, Appleby T, Vo T, Maderna A, Vernier JM, Hamatake R, Miner JN, Quart B. RDEA119/BAY 869766: a potent, selective, allosteric inhibitor of MEK1/2 for the treatment of cancer. Cancer Res. 2009 Sep 1;69(17):6839-47. doi: 10.1158/0008-5472.CAN-09-0679. Epub 2009 Aug 25. PubMed PMID: 19706763.

​Name: Binimetinib (MEK-162)
CAS#: 606143-89-9
Chemical Formula: C17H15BrF2N4O3
Exact Mass: 440.02956
Molecular Weight: 441.22681
Elemental Analysis: C, 46.28; H, 3.43; Br, 18.11; F, 8.61; N, 12.70; O, 10.88
 
EOS Med Chem produce Binimetinib (MEK-162),606143-89-9 in GMP plant, C-GMP standard, now COA, NMR, HPLC, MS is ok.
Binimetinib (MEK-162),606143-89-9 Intermediates, EOS Med Chem have 8; Binimetinib (MEK-162),606143-89-9 Impurity we have 10, all from GMP, FDA plant.
Now Binimetinib (MEK-162),606143-89-9 DMF document is preparing.
Until 2016, Aug, Binimetinib (MEK-162),606143-89-9 more than produced 25kg API, 120kg Intermediates

GMP PRODUCE:

Alectinib;Veliparib;Acalabrutinib;Venetoclax;Sotagliflozin;Ledipasvir;LX1606;Anacetrapib;Abemaciclib 

2016 Mumbai CPHI, Hope to meet!

2016 Barcelona CPHI, Hope to meet!

2016 Korea(한국) CPHI, C40, Welcome!

2016 Shanghai CPHI, W5C47, Welcome!

EOS Med Chem, Medchem is Big

執大象，天下往，往而無害，安平泰

網址: www.eosmedchem.com 

郵箱: gutian@eosmedchem.com; eosmedchem@gmail.com 

辦公室: 0086-531-69905422-806(直通)

攜帶番號 & WhatsApp: +8618653174435

Skype: willgutian

 
Binimetinib Binimetinib 606143-89-9
Binimetinib Intermediates MEK-162; ARRY-162; ARRY-438162; 606143-89-9
Binimetinib Intermediates Methyl 4-amino-2-((4-bromo-2-fluorophenyl)amino)-3-fluoro-5-nitrobenzoate
Binimetinib Intermediates Methyl 6-((4-bromo-2-fluorophenyl)amino)-7-fluoro-1H-benzo[d]imidazole-5-carboxylate 606143-48-0
Binimetinib Intermediates 5-((4-bromo-2-fluorophenyl)amino)-4-fluoro-1-methyl-1H-benzo[d]imidazole-6-carboxylic acid 1415564-99-6
Binimetinib Intermediates Methyl 5-((4-bromo-2-fluorophenyl)amino)-4-fluoro-1-methyl-1H-benzo[d]imidazole-6-carboxylate 1415559-93-1
 
 
Description: Binimetinib, also known as MEK162 (ARRY-162), is an oral, highly selective MEK inhibitor. In preclinical studies, MEK162 showed significant antitumor activities in cell lines and animal models. MEK162 is the first targeted therapy to show activity in patients with NRAS -mutated melanoma and might offer a new option for a cancer with few effective treatments.
Synonym: MEK162; MEK-162; MEK 162; ARRY162; ARRY-162; ARRY 162; ARRY438162, Binimetinib
IUPAC/Chemical Name: 5-((4-bromo-2-fluorophenyl)amino)-4-fluoro-N-(2-hydroxyethoxy)-1-methyl-1H-benzo[d]imidazole-6-carboxamide.
SMILES Code: O=C(C1=C(NC2=CC=C(Br)C=C2F)C(F)=C3N=CN(C)C3=C1)NOCCO
 
1: Hamidi H, Lu M, Chau K, Anderson L, Fejzo M, Ginther C, Linnartz R, Zubel A, Slamon DJ, Finn RS. KRAS mutational subtype and copy number predict in vitro response of human pancreatic cancer cell lines to MEK inhibition. Br J Cancer. 2014 Aug 28. doi: 10.1038/bjc.2014.475. [Epub ahead of print] PubMed PMID: 25167228.
2: Rebecca VW, Alicea GM, Paraiso KH, Lawrence H, Gibney GT, Smalley KS. Vertical inhibition of the MAPK pathway enhances therapeutic responses in NRAS-mutant melanoma. Pigment Cell Melanoma Res. 2014 Aug 11. doi: 10.1111/pcmr.12303. [Epub ahead of print] PubMed PMID: 25130256.
3: Urner-Bloch U, Urner M, Stieger P, Galliker N, Winterton N, Zubel A, Moutouh-de Parseval L, Dummer R, Goldinger SM. Transient MEK inhibitor-associated retinopathy in metastatic melanoma. Ann Oncol. 2014 Jul;25(7):1437-41. doi: 10.1093/annonc/mdu169. Epub 2014 May 26. PubMed PMID: 24864047.
4: Küsters-Vandevelde HV, Willemsen AE, Groenen PJ, Küsters B, Lammens M, Wesseling P, Djafarihamedani M, Rijntjes J, Delye H, Willemsen MA, van Herpen CM, Blokx WA. Experimental treatment of NRAS-mutated neurocutaneous melanocytosis with MEK162, a MEK-inhibitor. Acta Neuropathol Commun. 2014 Apr 8;2(1):41. doi: 10.1186/2051-5960-2-41. PubMed PMID: 24713450; PubMed Central PMCID: PMC4023633.
5: Thumar J, Shahbazian D, Aziz SA, Jilaveanu LB, Kluger HM. MEK targeting in N-RAS mutated metastatic melanoma. Mol Cancer. 2014 Mar 4;13:45. doi: 10.1186/1476-4598-13-45. PubMed PMID: 24588908; PubMed Central PMCID: PMC3945937.
6: Gritsman K, Yuzugullu H, Von T, Yan H, Clayton L, Fritsch C, Maira SM, Hollingworth G, Choi C, Khandan T, Paktinat M, Okabe RO, Roberts TM, Zhao JJ. Hematopoiesis and RAS-driven myeloid leukemia differentially require PI3K isoform p110α. J Clin Invest. 2014 Apr 1;124(4):1794-809. doi: 10.1172/JCI69927. Epub 2014 Feb 24. PubMed PMID: 24569456; PubMed Central PMCID: PMC3973083.
7: Miller CR, Oliver KE, Farley JH. MEK1/2 inhibitors in the treatment of gynecologic malignancies. Gynecol Oncol. 2014 Apr;133(1):128-37. doi: 10.1016/j.ygyno.2014.01.008. Epub 2014 Jan 14. Review. PubMed PMID: 24434059.
8: Chen X, Wu Q, Tan L, Porter D, Jager MJ, Emery C, Bastian BC. Combined PKC and MEK inhibition in uveal melanoma with GNAQ and GNA11 mutations. Oncogene. 2013 Oct 21. doi: 10.1038/onc.2013.418. [Epub ahead of print] PubMed PMID: 24141786.
9: Davar D, Tarhini AA, Kirkwood JM. Adjuvant immunotherapy of melanoma and development of new approaches using the neoadjuvant approach. Clin Dermatol. 2013 May-Jun;31(3):237-50. doi: 10.1016/j.clindermatol.2012.08.012. Review. Erratum in: Clin Dermatol. 2013 Jul-Aug;31(4):501. PubMed PMID: 23608443; PubMed Central PMCID: PMC3654101.
10: Akinleye A, Furqan M, Mukhi N, Ravella P, Liu D. MEK and the inhibitors: from bench to bedside. J Hematol Oncol. 2013 Apr 12;6:27. doi: 10.1186/1756-8722-6-27. Review. PubMed PMID: 23587417; PubMed Central PMCID: PMC3626705.