Pharmaceutical feminizing HRT

Generally speaking, every MTF HRT regimen will include an anti-androgen, to suppress the effects of testosterone on the body, alongside some form of estrogen and some form of progesterone. However, depending on health condition and the effects you're going for, your needs may vary. This is a collection of a few HRT regimens I've found interesting or representative.

Basic: Spironolactone + 17β-estradiol
Spironolactone serves as the anti-androgen. It binds to the Androgen Receptor (AR), preventing Testosterone/DHT from activating the receptor, but as an 'antagonist'/'partial agonist' it doesn't "turn on" the AR to a significant degree. Estradiol, also known as E2, is one of the body's natural estrogens. It activates the Estrogen receptors.

Epigenetic change reversal with Bicalutamide or Mifepristone
Some androgen receptor antagonists, such as mifepristone or potentially bicalutamide, actually have the ability to cause the androgen receptor to start recruiting corepressors instead of coactivators, which may undo the irreversible or slowly reversible changes in gene expression caused by the AR. While further research is needed, it appears that other anti-androgens don't cause corepressors to be recruited by the AR, or they still prevent the translocation of the AR from the cytosol into the nucleus. The following plan bears many similarities to the hormone therapy used for prostate cancer.

Here's an example plan:
 * 1) Measure PSA levels as a baseline measurement of the expression of androgen-dependent genes, as well as free/bound T levels.
 * 2) Nil out bodily production of testosterone using GnRH agonists/antagonists, so that available androgen receptors are mostly in the cytosol. Wait 1-2 weeks for magic to happen.
 * 3) Measure PSA and T levels again. Low T levels should confirm that testosterone is no longer actively circulating, so new androgen receptors are sitting bored in the cytosol waiting for somebody to come bind to them. Existing androgen receptors may still be in the nucleus! PSA levels should be trending downwards due to ARs slowly going away, but not nil yet.
 * 4) Run a course of bicalutamide or mifepristone. This will bind to the ARs in the cytosol, bring them into the nucleus and start assembling the AR protein complex around the AREs (e.g. the promoter and the enhancer PSA gene AREs.) However, in the absence of T, corepressors will be attached to the AR rather than coactivators. Thus, the histones will be deactivated and the androgen-dependent genes such as PSA will no longer be expressed.
 * 5) Measure PSA levels again. PSA should be near nil before moving to the next step.
 * 6) Discontinue bicalutamide or mifepristone. At this point, the epigenetic changes should have been undone! Additionally, any testosterone left should have been kicked out of the ARs by bicalutamide/mifepristone, and degraded via aromatase.
 * 7) GnRH antagonists can now be withdrawn (since they're crazy expensive), and replaced with an anti-androgen which prevents the translocation of the ARs into the nucleus (e.g. cyproterone), or even spironolactone + estradiol, as long as T levels remain safely in cis female ranges.

Add estradiol or progesterone to taste at any point in this therapy, since those don't interact.

Covering the gaps
If you start HRT past your early 20s, your final breast size will probably be a cup size or two smaller than your close relatives. Besides surgical breast augmentation, there are a few hormonal things to try.

Resources

 * WPATH Standards of Care contains "diagnostic criteria", medical treatment recommendations, timelines etc.
 * Hormones: a guide for MTFs is a great, human-readable guide on what to expect from hormonal transition.