This is to elaborate on Dr. Peterson's quite correct translation.
The term "hard endpoint" is used in contradistinction to "surrogate endpoint".

See Wikipedia's explanation:
In clinical trials, a surrogate endpoint is a measure of effect of a certain treatment that may correlate with a real endpoint but has no guaranteed relationship.

It is a major issue in testing the efficacy of medication. For example, most cholesterol-lowering drugs (e.g. the statins) are used to control cardiovascular disease, yet they were introduced with only information on their capacity to decrease cholesterol levels. While elevated cholesterol levels increase the likelihood for heart disease, the relationship is not linear - many people with normal cholesterol develop heart disease, and many with high cholesterol do not. In the case of simvastatin (Zocor®), proof of its efficacy in reducing cardiovascular disease was only presented five years after its original introduction, and then only for secondary prevention. In another case, AstraZeneca has been accused of marketing rosuvastatin (Crestor®) without providing hard endpoint data, relying instead on surrogate endpoints. The company counters that it had been tested on larger groups of patients than any other drug in the class, and that its effects should be comparable to the other statins.

Back to my own explanation.
Say you are evaluating a medicine for stomach ulcers. One might think that proof that a medicine raises the pH of the stomach contents is proof that it helps prevent ulcers. Well, maybe it does and maybe it doesn't. The stomach contents acidity is in fact a "surrogate endpoint". The "hard endpoint" would be the actual development of an ulcer vs the absence of an ulcer after a fixed period of time. A "hard endpoint" is preferable in any clinical trial.