Interactions
Amoxicillin may interact with these drugs:

Anticoagulants (dabigatran, warfarin). Cancer treatment (methotrexate). Uricosuric drugs. Typhoid vaccine
Probenecid reduces renal excretion and increases the blood levels of amoxicillin. Oral contraceptives may become less effective. Allopurinol (gout treatment). Pharmacology
Amoxicillin (α-amino-p-hydroxybenzyl penicillin) is a semisynthetic derivative of penicillin with a structure similar to ampicillin but with better absorption when taken by mouth, thus yielding higher concentrations in blood and in urine. Amoxicillin diffuses easily into tissues and body fluids. It will cross the placenta and is excreted into breastmilk in small quantities. It is metabolized by the liver and excreted into the urine. It has an onset of 30 minutes and a half-life of 3.7 hours in newborns and 1.4 hours in adults.Amoxicillin attaches to the cell wall of susceptible bacteria and results in their death. It also is a bactericidal compound. It is effective against streptococci, pneumococci, enterococci, Haemophilus influenzae, Escherichia coli, Proteus mirabilis, Neisseria meningitidis, Neisseria gonorrhoeae, Shigella, Chlamydia trachomatis, Salmonella, Borrelia burgdorferi, and Helicobacter pylori. As a derivative of ampicillin, amoxicillin is a member of the penicillin family and, like penicillins, is a β-lactam antibiotic. It inhibits cross-linkage between the linear peptidoglycan polymer chains that make up a major component of the bacterial cell wall. It has two ionizable groups in the physiological range (the amino group in alpha-position to the amide carbonyl group and the carboxyl group). History
Amoxicillin was one of several semisynthetic derivatives of 6-aminopenicillanic acid (6-APA) developed by the Beecham Group in the 1960s.
Infantile neuronal ceroid lipofuscinoses (INCL) or Santavuori disease or Hagberg-Santavuori disease or Santavuori-Haltia disease or Infantile Finnish type neuronal ceroid lipofuscinosis or Balkan disease is a form of NCL and inherited as a recessive autosomal genetic trait. The disorder is progressive, degenerative and fatal, extremely rare worldwide – with approximately 60 official cases reported by 1982, perhaps 100 with the condition in total today – but relatively common in Finland due to the local founder effect. Presentation
The development of children born with INCL is normal for the first 8–18 months, but will then flounder and start to regress both physically and mentally. Motor skills and speech are lost, and optic atrophy causes blindness. A variety of neurological symptoms, such as epilepsy and myoclonic seizures, appear. The senses of hearing and touch remain unaffected. The average lifespan of an INCL child is 9–11 years. Causes
It has been associated with palmitoyl-protein thioesterase. Diagnosis
Treatment
Treatment is limited. Drugs can alleviate the symptoms, such as sleep difficulties and epilepsy. Physiotherapy helps affected children retain the ability to remain upright for as long as possible, and prevents some of the pain. Recent attempts to treat INCL with cystagon have been unsuccessful. See also
FAIDD (The Finnish Association on Intellectual and Developmental Disabilities)

References
External links

GeneReviews/NCBI/NIH/UW entry on Neuronal Ceroid-Lipofuscinosis
An overview (in Finnish)
The INCL organization of Finland (in Finnish)