Mechanisms of action of EGFR inhibitors

Understanding the mechanisms of action of EGFR inhibitors in NSCLC: what we know and what we do not know

Lung Cancer ◽

10.1016/s0169-5002(03)00135-1 ◽

2003 ◽

Vol 41 ◽

pp. 15-22 ◽

Cited By ~ 7

Author(s):

David Raben ◽

Barb Helfrich ◽

Fortunato Ciardiello ◽

Paul A. Bunn

Keyword(s):

Mechanisms Of Action ◽

Egfr Inhibitors

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Case Formulation and Design of Behavioral Treatment Programs

European Journal of Psychological Assessment ◽

10.1027//1015-5759.19.3.164 ◽

2003 ◽

Vol 19 (3) ◽

pp. 164-174 ◽

Cited By ~ 27

Author(s):

Stephen N. Haynes ◽

Andrew E. Williams

Keyword(s):

Functional Analysis ◽

Behavior Problems ◽

Behavioral Treatment ◽

Clinical Case ◽

Relative Magnitude ◽

Mechanisms Of Action ◽

Treatment Programs ◽

Case Formulation ◽

Functional Relations ◽

Causal Variables

Summary: We review the rationale for behavioral clinical case formulations and emphasize the role of the functional analysis in the design of individualized treatments. Standardized treatments may not be optimally effective for clients who have multiple behavior problems. These problems can affect each other in complex ways and each behavior problem can be influenced by multiple, interacting causal variables. The mechanisms of action of standardized treatments may not always address the most important causal variables for a client's behavior problems. The functional analysis integrates judgments about the client's behavior problems, important causal variables, and functional relations among variables. The functional analysis aids treatment decisions by helping the clinician estimate the relative magnitude of effect of each causal variable on the client's behavior problems, so that the most effective treatments can be selected. The parameters of, and issues associated with, a functional analysis and Functional Analytic Clinical Case Models (FACCM) are illustrated with a clinical case. The task of selecting the best treatment for a client is complicated because treatments differ in their level of specificity and have unequally weighted mechanisms of action. Further, a treatment's mechanism of action is often unknown.

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Enkephalin influences on behavioral and neural plasticity: Mechanisms of action.

PsycEXTRA Dataset ◽

10.1037/e474102004-001 ◽

1990 ◽

Cited By ~ 1

Author(s):

Joe L. Martinez ◽

Patricia H. Janak ◽

Susan B. Weinberger ◽

Gery Schulteis

Keyword(s):

Neural Plasticity ◽

Mechanisms Of Action

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The diabetic wound healing effect of a two-herb formula and its mechanisms of action

Planta Medica ◽

10.1055/s-0032-1320306 ◽

2012 ◽

Vol 78 (11) ◽

Author(s):

CBS Lau ◽

VKM Lau ◽

CL Liu ◽

PKK Lai ◽

JCW Tam ◽

...

Keyword(s):

Wound Healing ◽

Mechanisms Of Action ◽

Diabetic Wound ◽

Healing Effect ◽

Diabetic Wound Healing ◽

Wound Healing Effect

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Mechanisms of action of antihyperglycemic mexicanolides isolated from Swietenia humillis: in vivo and in silico approaches

Planta Medica ◽

10.1055/s-0036-1596301 ◽

2016 ◽

Vol 81 (S 01) ◽

pp. S1-S381 ◽

Cited By ~ 1

Author(s):

B Ovalle-Magallanes ◽

A Madariaga-Mazón ◽

A Navarrete ◽

R Mata

Keyword(s):

In Silico ◽

Mechanisms Of Action

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Inhibition of the Activities of α2-Plasmin inhibitor (PI) and CI inhibitor (CI-Inh) by the Synthetic Fibrinolytic Agent, 3-Hydroxypropyl Flufenamide (Flu-HPA)

10.1055/s-0038-1665785 ◽

1979 ◽

Author(s):

L Miles ◽

J Burnier ◽

M Verlander ◽

M Goodman ◽

A Kleiss ◽

...

Keyword(s):

Plasminogen Activators ◽

Inhibitory Effect ◽

Mechanisms Of Action ◽

Flufenamic Acid ◽

Clot Lysis ◽

Factor Xiia ◽

Dependent Inhibition ◽

Normal Human ◽

Plasmin Inhibitor

Flu-HPA is one of a series of flufenamic acid derivations that enhances plasminogen-dependent clot lysis in vitro. Studies of possible mechanisms of action of Flu-HPA were undertaken. The influence of Flu-HPA on the inhibition of purified plasmin by purified PI was studied. PI activity was assessed by its inhibition of the clevage of the tripeptide S-2251 (H-D-Val-Leu-Lys-pNA) by plasmin. Flu-HPA was dissolved in DMF or in methonol and preincubated with PI before addition of plasmin. At Flu-HPA concentrations greater than 1mM and up to 60mM, the inhibitory activity of PI was totally lost. The inhibitory effect of normal human plasma on plasmin was also completely abolished at concentrations of Flu-HPA between 2.5 and 40mM. The effect of Flu-HPA on the inhibition of purified plasma kallikrein by purified CI-Inh was also studied. CI-Inh activity was measured by its inhibition of cleavage of the tripeptide Bz-Pro-Phe-Arg-pNA by kallikrein. When Flu-HPA, dissolved in DMF or in methonol, was preincubated with CI-Inh, a concentration dependent inhibition of CI-Inh activity was observed. CI-Inh activity was abolished by concentrations of Flu-HPA greater than 1mM. Flu-HPA also inhibited the activity of CI-Inh on purified Factor XIIa. These observations suggest that this flufenamic acid derivative may enhance fibrinolysis not only by inhibiting PI activity but also by decreasing the inactivation of plasminogen activators by CI-Inh.

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