Bufotoxins are a family of toxic steroid lactones or substituted Tryptamines of which some may or may not be toxic. They occur in the parotoid glands, skin and poison of many toads (genus Bufo) and other amphibians, and in some plants and mushrooms. The exact composition varies greatly with the specific source of the toxin. It can contain 5-MeO-DMT, bufagins, bufalin, bufotalin, bufotenin, bufothionine, dehydrobufotenine, epinephrine, norepinephrine, and serotonin. Some authors have also used the term bufotoxin  to describe the conjugate of a bufagin with suberylarginine.The toxic substances found in toads can be divided by chemical structure in two groups:

bufadienolides, which are cardiac glycosides (e.g., bufotalin, bufogenin)
tryptamine-related substances (e.g., bufotenin)Toads known to secrete bufotoxin include the following:
Bufo alvarius
Bufo americanus
Bufo arenarum
Bufo asper
Bufo blombergi
Bufo boreas
Bufo bufo
Bufo bufo gargarizans
Sclerophrys gutturalis (syn. Bufo gutturalis)
Bufo formosus
Bufo fowleri
Rhinella marina (formerly Bufo marinus)
Bufo melanostictus
Bufo peltocephalus
Bufo quercicus
Bufo regularis
Bufo valliceps
Bufo viridis
Bufo vulgaris

Extraction
Extract from the skin of certain Asian toads, such as Bufo bufo gargarizans and Bufo melanostictus, is often found in certain Chinese folk remedies. The Pharmacopoeia of the Peoples Republic of China (ChP) considers the two species valid sources of toad venom (Chinese: 蟾酥; pinyin: Chánsū; Latin: bufonis venenum), and requires the dry product to contain at least 6% of cinobufagin and resibufogenin combined by weight. The extract is obtained by squeezing the parotoid glands of caught, washed toads for a white venom and drying; the final dried venom is usually brown, with a chunk or flake form. Human poisoning
Toad‐venom poisoning is rare but can kill.
It can also cause severe hypertension (high blood pressure) when combined with sympathomimetic drugs or MAO-A inhibitors, bradycardia (low heart rate) when combined with antiarrhythmics or mefloquine, and hypoglycemia (low blood sugar) when combined with antidiabetic drugs such as insulin. Pharmacology
Mechanism of action
Levobunolol is a non-cardioselective beta blocker, that is, it blocks beta-1 receptors as well as beta-2 receptors. The latter type dominates in the ciliary body, where it controls aqueous humour production. Blocking this type of receptor reduces aqueous humour production, lowering intraocular pressure. The substance has no relevant membrane stabilizing effect or intrinsic sympathomimetic activity. Like other beta blockers, and unlike the anti-glaucoma medication pilocarpine, levobunolol has no effect on accommodation and pupil size. Pharmacokinetics
The substance quickly penetrates the cornea and reaches the aqueous humour. It is reduced to dihydrolevobunolol, which is equally active, in the eyes tissues. The drug starts to lower intraocular pressure within an hour, reaches its maximum effect after two to six hours, and remains effective for up to 16 hours. It has an elimination half-life of six hours and is mainly excreted via the kidney. Chemistry
Levobunolol is the pure L-enantiomer of bunolol and has more than 60 times the pharmacological activity of D-bunolol. It is used as the hydrochloride, which melts at 209 to 211 °C (408 to 412 °F) and is soluble in water and methanol and slightly soluble in ethanol. References

Ishibashi T, Yokoi N, Kinoshita S (2003). "Comparison of the effects of topical levobunolol and timolol solution on the human ocular surface". Cornea. 22 (8): 709–15. doi:10.1097/00003226-200311000-00001.