During the two 'off' weeks, an ECA stack can be used as required. ECA will not cause such a pronounced down regulation and desensitization of the receptors, certainly not to the extent of clen. Ephedrine has a short half life in contrast to clen which results in times throughout the day where the betas will partially recover from stimulation by adrenaline and nor-adrenaline. Potency is also much weaker that that of clen, as it is not a specific agonist. Ephedrine is also thought to increase the conversion of endogenous/exogenous T4 to T3 through the activation of deiodinase enzymes responsible for this process. This is important as clen is known to slow the rate of T4 to T3 conversion. As a side note, some bodybuilders will use T3 concurrently with the Clenbuterol/ECA cutting cycle (together with certain anabolic/androgenic steroids no doubt!) in an attempt to at least maintain plasma T3 levels.
The mechanism of ISGylation and deISGylation is similar to that of ubiquitin , although the complete system components have not yet been identified. The activating E1 enzyme (UBE1L) charges ISG15 by forming a high-energy thiolester intermediate and transfers it to the UbcH8 E2 protein. UbcH8 has been identified as the major E2 for ISGylation, although it also functions in ubiquitination. The E2 protein subsequently transfers the ISG15 to specific E3 ligases (Herc5  ) and relevant intracellular substrates. Only one deconjugating protease with specificity to ISG15 has been identified to date: UBP43 (a member of the USP family) cleaves ISG15-peptide fusions and also removes ISG15 (deISGylation) from native conjugates.