Acids with exotic components are difficult to store in biological systems and difficult to synthesize - where is an animal going to find fluorine and antimony?
But worse: a cloud of flame or of acid does not have much knockdown power. People who are doused in gasoline can go running off and jump in a pool. Later on it is very bad for them and they will likely die of their burns but acutely it is not a good way to make something stop moving so it can be eaten. Even if the flame / acid blinds the animal it will still go running off and will fight you if it feels you.
Snakes do it up as regards knockdown power. A dragon could be a snake. A flying snake with a venom breath weapon would be formidable. Spitting snakes are exactly this except not flying.
Your dragon sprays a mist of venom which combines tissue destructive enzymes and anticoagulants. The showy and fantastic result: after breathing this venom, two or three coughs later the target animal explosively exsanguinates from massive pulmonary hemorrhage.
You do not need to invent much to come up with a venom that could do this. Info on snake venom pasted below with more at source.
Haemotoxic snake venoms: their functional activity, impact on snakebite victims and pharmaceutical promise
Often, extensive local tissue damage develops (Fig 2), characterised
by necrosis of the affected limb and requiring surgical debridement or
amputation if left untreated. Hydrolytic enzymes, such as snake venom
metalloproteinases (SVMPs) and PLA2s, and non‐enzymatic cytotoxic
3FTXs have been implicated as the causative agents found in different
snake venoms (Escalante et al, 2009; Rivel et al, 2016). Recently it
was shown that the destruction of local tissue may also be promoted by
snake venom inducing the formation of neutrophil extracellular traps
(NETs), which in turn block blood vessels and contain the venom toxins
to bite site, thereby promoting cytotoxic pathology (Katkar et al,
2016)... Haemorrhage caused by snake venom is often complicated and
exacerbated by patients presenting with blood clotting disturbances as
the result of venom‐induced consumption coagulopathy (VICC). VICC, a
disseminated intravascular coagulation (DIC)‐like syndrome, is
characterised by low or undetectable levels of fibrinogen, resulting
in incoagulable blood (Fig 2) (Isbister, 2010; Maduwage & Isbister,