Cardiovascular Toxicity (QT Prolongation) In Drug Development Overview

Nobody working in drug development can fail to beThe tests most commonly used are the hERG binding
aware of the issue that is QT prolongation, howeverassay and Rubidium flux tests
some people are finding they need a little moreIn terms of Ex-vivo models the most popular are
information if they are going to tackle and plan for itpukinji fiber tests and isolated heart tests, these
within their drug development programmes.whole tissue and whole organ tests are expensive
There are three main ways that cardiovascularbut do provide a lot more information on what is
toxicity can present itself:going on and provide a wider insight.
In-vivo tests include dogs, non-human-primates, and
1. Changes to heart ratepigs, rodents are not a good model for the human
2. Changes to conductivity within the heartheart and should not be used. Again the expense of
3. Changes to the repolarization of the heart (QTthese models is made up for by the excellent data
prolongation)they provide. The studies are generally conducted in
It is this QT prolongation that is obviously theconscious animals which are remotely monitored,
hottest issue and is a consequence of impacting thesingle dose cross over study designs are used, time
repolarization of the cardiomyocytes. The pathway isand duration of effect is looked for and compared
the hERG channels are blocked, which increased thewith systemic drug levels. Heart rate, ECG, Blood
action potential of the cells in the heart, which in turnPressure, Body Temperature, and activity levels are
causes the QT prolongation.all monitored.
This problem has been seen in a large number ofOne of the most important things to look at is left
drugs and has impacted on a great many drugventricular pressure as this gives the greatest insight
development programmes, from complete removalinto normal function, Charles Rivers have done a
of a drug from the market, to prescribing restrictions,great deal of work to validate this with Atenolo and
delays in approval and a huge number of drugs killedPimobedam. With both drugs systolic BP, diastolic BP
at an early stage. It is also worth noting that there isand heart rate remained the same but changes in left
not a pattern to those drugs affected and it appearsventricular pressure alluded to issues that needed to
to affect a large number of different drugs.be addressed.
But what can be done to manage this risk? WellThere are two guidelines that need to be referred to
there are a wide variety of early discovery screens,when planning these studies ICH57A (general safety
In-vitro, Ex-vivo, and In-vivo.pharmacology) and ICH57B (Specific QT prolongation
The most common In-vitro study is the Patch Clampregulations).
- this is actually the gold standard study and involvesWhen assessing the Pre-clinical it is important to take
measuring the current through the hERG channel (Ikra good look at the data and consider the following;
Chanel) to give an IC50 for the drug, this IC50 willwhat was actually observed as the assays are not
give you an indication if you are going to see effects100% effective, any small flags will impact on clinical
at therapeutic dose levels. Whilst this is the goldtrial design, how will the expected PK/PD profiles
standard it is not a test that lends itself well to highimpact on the results, will you expect patients to get
throughput screening.into affected dose levels?
Another test is the hERG binding assay, this is aBefore commencing human trials there are guidelines
competitive assay that tests your drug against athat need to be considered ICH E14 which gives
radio labeled standard, this is a good test which caninstruction on the evaluation of QT prolongation in
be used in high throughput screening, and is wellman, in some regions its now compulsory, but in
correlated to the Patch Clamp test.others you can argue away from it with pre-clinical
Another is the Rubidium Flux assay, where you loaddata. In the clinic QT prolongation is tested in healthy
the cells with rubidium add your compound and KCl,volunteers at therapeutic doses and multiples thereof,
this allows you to measure the rubidium excretedmetabolic inhibition may be needed to raise drug
from the cell and from this judge hERG channellevels levels high enough, positive controls are also
activity. This once again lends itself to even fastused (moxifloxacin).
screening but there is some drop off in relation toWhere QT prolongation is seen the following
the gold standard.guidelines are provided:
The final test is the membrane potential dye test,- 6-10 msec unlikely risk
where cells are loaded with dye and as the hERG- >10 msec possible risk
channel functions dye is flushed from the cell, this isThese regulations are the same for cardiovascular
the fastest test but least accurate.drugs as for other therapy areas.