Editing Synergy (section)

=== Drug synergy ===
{{also|Codrug#Common codrugs|Combination drug#Common combination drugs}}

Mechanisms that may be involved in the development of synergistic effects include:
*Effect on the same cellular system (e.g. two different [[antibiotics]] like a [[penicillin]] and an [[aminoglycoside]]; penicillins damage the cell wall of gram-positive [[bacteria]] and improve the penetration of aminoglycosides).<ref name = "Tripathi_2013">{{cite book | vauthors = Tripathi KD |title=Essentials of medical pharmacology |date=2013 |location=New Delhi | publisher = JP Medical Ltd |isbn=9789350259375 |edition=Seventh }}</ref>{{rp|698}}
*[[Bioavailability]] (e.g. [[ayahuasca]] (or [[pharmahuasca]]) consists of [[N,N-Dimethyltryptamine|DMT]] combined with [[Monoamine oxidase inhibitor|MAOIs]] that interfere with the action of the MAO enzyme and stop the breakdown of chemical compounds such as DMT).
*Reduced risk for [[substance abuse]] (e.g. [[lisdexamfetamine]], which is a combination of the [[amino acid]] [[Lysine|<small>L</small>-lysine]], [[covalently bonded|attached to]] [[dextroamphetamine]], may have a lower liability for abuse as a recreational drug)
*Increased potency (e.g. as with other [[Nonsteroidal anti-inflammatory drug|NSAIDs]], [[Compound analgesic|combinations]] of aspirin and [[caffeine]] provide slightly greater pain relief than aspirin alone.<ref name=pmid22419343>{{cite journal | vauthors = Derry CJ, Derry S, Moore RA | title = Caffeine as an analgesic adjuvant for acute pain in adults | journal = The Cochrane Database of Systematic Reviews | volume = 3 | issue = 3 | pages = CD009281 | date = March 2012 | pmid = 22419343 | doi = 10.1002/14651858.CD009281.pub2 | s2cid = 205199173 | veditors = Derry S }}</ref>).
*Prevention or delay of degradation in the body (e.g. the antibiotic [[Ciprofloxacin]] inhibits the metabolism of [[Theophylline]]).<ref name = "Tripathi_2013" />{{rp|931}}
*Slowdown of excretion (e.g. [[Probenecid]] delays the [[renal]] excretion of Penicillin and thus prolongs its effect).<ref name = "Tripathi_2013" />{{rp|931}}
*Anticounteractive action: for example, the effect of [[oxaliplatin]] and [[irinotecan]]. Oxaliplatin [[wikt:intercalation|intercalates]] DNA, thereby preventing the cell from replicating DNA. Irinotecan inhibits [[topoisomerase 1]], consequently the cytostatic effect is increased.<ref name="Jia_2009">{{cite journal | vauthors = Jia J, Zhu F, Ma X, Cao Z, Cao ZW, Li Y, Li YX, Chen YZ | title = Mechanisms of drug combinations: interaction and network perspectives | journal = Nature Reviews. Drug Discovery | volume = 8 | issue = 2 | pages = 111–28 | date = February 2009 | pmid = 19180105 | doi = 10.1038/nrd2683 | s2cid = 54466254 }}</ref>
*Effect on the same receptor but different sites (e.g. the coadministration of benzodiazepines and barbiturates, both act by enhancing the action of GABA on GABA<sub>A</sub> receptors, but benzodiazepines increase the frequency of channel opening, whilst barbiturates increase the channel closing time, making these two drugs dramatically enhance GABAergic neurotransmission).{{citation needed|date=May 2018}}
* In addition to the chemical nature of the drug itself, the topology of the chemical reaction network that connect the two targets determines the type of drug-drug interaction.<ref>Mehrad Babaei et al., Biochemical reaction network topology defines dose-dependent Drug–Drug interactions. Comput Biol Med 155:106584 (2023)  doi: 10.1016/j.compbiomed.2023.106584</ref> 

More mechanisms are described in an exhaustive 2009 review.<ref name="Jia_2009"/>