It's my understanding the main hormone involved in morphing (in fact metamorphosis to give it its full title) is thyroxine or tri-iodothyronine which is derived from thyroxine but stress hormones (Cortisone and related compounds) play a role and work with thyroxine in amphibian metamorphosis. In most amphibians stress triggers cortisone and this causes early metamorphosis. A larva will stay aquatic longer if conditions are good.
Axolotls have a genetic block of the thyroid stimulating hormone which triggers the growth of the thyroid and prevents thyroxine manufacture and are generally very resistant to morphing. Trying to induce morphing by stressing them such as drying them out is more likely to kill them than overcome the metabolic block.
As always there are a few exceptions, possibly animals with a mutant gene permitting thyroid hormone development.
A great deal of knowledge of development as well as understanding of thyroid and pituitary function has resulted from work on amphibians.
Axolotls metamorphose easily and reliably if placed in water containing thyroxine, but if the axolotl is too young you get a very small and difficult to raise salamander, if done too late you get a large and very short lived salamander or one that dies in morphing and if done at a time and size approximating to tiger salamander metamorphosis you get a handsome salamander which has a greatly reduced life expectancy compared with a normal axolotl, and has lost that wonderful ability to repair injuries without scarring.
An adult axolotl is to all intents and purposes a sexually mature larva - the technical term is neoteny. When morphed they presumably can be in both non-breeding and breeding form.
It is possible, by giving anti-thyroid drugs, to prevent almost all amphibians metamorphosing, for instance producing giant xenopus tadpoles which eventually develop sexually despite being in larval form. If the treatment is stopped, because their skeletons have ossified in the larval form you do not get a normal adult.