It appears the human digestive system metabolizes niclosamide primarily
though the enzymes  CYP1A2 and UGT1A1.  As was discovered years
ago, through the use of grapefruit juice to mask the taste of a particular
medication, its enzyme inhibitors can also have a troublesome impact on the absorption and
serum levels of many drugs.  Might niclosamide’s poor solubility be
just one part of the problem, with enzyme metabolism more critical?

Consider the possibility of inhibiting enzymes CYP1A2 and UGT1A1
through the early p.o.administration of select drugs and supplements,
prior to ingestion of niclosamide.  For example, cimetidine  and melatonin
are proven, relatively benign inhibitors of CYP1A2.  (Ciprofloxacin inhibits
CYP1A2 as well but with more possible side effects). Acetacin, isolated
from turnera diffusa  (Damiana) and KaeminhibitUGT1A1.  

Another route - rectal suppository- though never mentioned in the literature, could also evade  its first-pass enzyme degradation. Many water-insoluble meds are administered via suppository.  Why not try niclosamide?