Famotidine in Dogs and Cats: A Clinical Reference

Bottom line

The 2018 ACVIM consensus statement on the rational administration of gastrointestinal protectants places proton pump inhibitors (PPIs), not H2-receptor antagonists, as standard of care for the medical treatment of gastroduodenal ulceration and erosion (GUE) in dogs and cats, and concludes that H2RA monotherapy given twice daily is inferior to twice-daily PPI treatment [1]. Canine intragastric-pH data match that ranking: oral famotidine held pH ≥3 for 22 ± 8% of the recording time versus 63 ± 14% for an omeprazole tablet [2]. Famotidine's effect also decays with continued twice-daily dosing: by treatment days 12 and 13 in dogs there were no significant differences in acid suppression between famotidine and placebo [3], and in cats it fell significantly by day 13 from a day-1 level that had never met the acid-suppression target in the first place [4]. The practical conclusion is not that famotidine is a bad drug, but that it is very often prescribed where acid suppression itself was never indicated.

Drug facts

Class and mechanism. Famotidine is a histamine type-2 receptor antagonist. H2RAs inhibit acid secretion by competitively blocking H-2 receptors on the parietal cell, thereby decreasing basal and meal-stimulated gastric acid secretion [1]. The blockade is competitive and reversible, and therefore surmountable, which is directly relevant to the tachyphylaxis discussed below.

Onset relative to a PPI. Famotidine acts on the first dose. PPIs do not: inhibition of acid secretion is approximately 30% of maximal on day 1 of administration because of incomplete binding to all H+/K+-ATPases, and maximal inhibitory effect is achieved within approximately 2-4 days [1]. Rapid onset is famotidine's one genuine pharmacologic advantage over a PPI.

Elimination. H2RAs are eliminated by a combination of renal excretion and hepatic metabolism [1]. In humans, 65 to 70% of an intravenous famotidine dose is recovered in the urine as unchanged compound [5].

Formulations. Famotidine injection is a human-label product supplied at 4 mg/mL, as a 20 mg/5 mL single-dose vial and 40 mg/10 mL and 200 mg/50 mL multi-dose vials [5]. Oral tablets and an oral suspension are separately marketed human-label products.

Label status. There is no veterinary-approved famotidine product. The ACVIM panel states that not a single agent discussed in the consensus statement is FDA-approved for use in dogs or cats [1]. Every dose below is therefore extra-label.

Contraindications and cautions. The human injection label contraindicates famotidine in patients with a history of serious hypersensitivity reactions, for example anaphylaxis, to famotidine or other H2-receptor antagonists, and carries warnings for CNS adverse reactions and for QT prolongation in moderate and severe renal impairment [5].

Famotidine versus omeprazole for acid suppression

For sustained acid suppression, oral omeprazole outperforms oral famotidine in both species, and the margin is wide.

In a randomized, 4-way crossover, open-label study in six healthy adult mixed-breed colony dogs, famotidine PO at 1.0-1.3 mg/kg q12h produced mean percent time (MPT) at intragastric pH ≥3 of 22 ± 8% and at pH ≥4 of 14 ± 6%, versus 63 ± 14% and 52 ± 17% for an omeprazole tablet at 1.5-2.6 mg/kg q24h, and 6 ± 6% and 5 ± 5% for placebo [2]. Both omeprazole formulations significantly increased intragastric pH compared with famotidine and placebo [2].

The consensus statement summarises the wider literature the same way. H2RAs are inferior to PPIs for increasing intragastric pH and for prevention of exercise-induced gastritis in dogs, and higher dosages of famotidine (1-1.3 mg/kg q12h) had only a weak effect on intragastric pH in healthy mixed-breed dogs [1]. The sled-dog literature shows both halves of the picture. Oral famotidine at 1 mg/kg q24h decreased the severity of gastric lesions in racing sled dogs compared with no treatment [1]. But in a similar study, omeprazole at 0.85 mg/kg PO q24h significantly decreased the severity and prevalence of gastric lesions compared with famotidine at 1.7 mg/kg PO q12h, in a randomized positive-control study of 52 dogs before and after a 300-mile race [1]. So famotidine beats nothing, but even at 1.7 mg/kg twice daily, nearly double the 1 mg/kg q24h that had beaten no treatment, it did not close the gap against omeprazole [1].

In cats, famotidine at 0.88-1.26 mg/kg PO q12h was significantly more efficacious than placebo but inferior to omeprazole in increasing intragastric pH in healthy colony cats [1].

Three consensus positions are worth having on hand when this comes up on rounds: there is a lack of benefit for administration of H2RAs on a once-daily basis in dogs and cats to treat GUE and reflux esophagitis; monotherapy with an H2RA given twice daily is inferior to PPI treatment given twice daily; and there is no evidence of benefit of administration of an H2RA with a PPI for ulcer healing, a combination that may diminish the effectiveness of the PPI [1].

The injectable picture is more favourable. In 12 healthy Beagles, famotidine at 0.5 mg/kg IV q12h significantly suppressed gastric acid secretion compared with saline solution, as did pantoprazole and omeprazole, whereas ranitidine at 2 mg/kg IV q12h did not [6]. That same study reported that twice-daily administration of a suspension of omeprazole was the only regimen tested that approached the potential therapeutic efficacy for acid-related disease when assessed by criteria used for human patients [6].

The strongest famotidine result anywhere in the veterinary literature is a constant-rate infusion. In nine healthy Beagle dogs given famotidine as a 1.0 mg/kg IV one-time loading bolus followed by a continuous infusion of 8.0 mg/kg/day, MPT at pH ≥3 was 92.1 ± 8.5, 96.3 ± 6.2 and 90.0 ± 15.7 on days 1, 2 and 3 respectively, versus 49.3 ± 27.3, 42.2 ± 19.6 and 45.8 ± 10.1 for famotidine 1.0 mg/kg IV q12h [7]. The authors concluded that a famotidine CRI, but not standard doses of famotidine, achieves the clinical goals established in people to promote healing of gastric tissue injury, and offers an alternative to intravenous treatment with proton pump inhibitors in dogs [7]. Note the boundary of that finding: three consecutive days, in healthy dogs. It does not establish whether a CRI escapes tachyphylaxis over a longer course.

Tachyphylaxis and loss of effect with repeated dosing

This is the single most clinically important famotidine-specific finding, and the reason an open-ended famotidine prescription quietly stops delivering what it delivered on day one.

Dogs. In a randomized, 2-factor repeated-measures crossover study, six healthy adult colony Beagles received oral placebo or famotidine 1.0 mg/kg q12h for 14 consecutive days, with intragastric pH recorded continuously on treatment days 1-2 and 12-13 [3]. Continued administration of famotidine resulted in a significant decrease in mean pH, MPT ≥3, and MPT ≥4 (P < .0001) on days 12 and 13, amounting to a mean decrease in pH of 1.63 on days 12 and 13 compared with days 1 and 2, and a mean decrease of MPT ≥3 and MPT ≥4 by 33 and 45% respectively over the same period [3]. The finding that should actually change prescribing is what that decay amounts to: by days 12 and 13 the gastric acid suppressing effects of famotidine declined significantly and failed to meet either pH goal for pH increase for humans in all dogs, and there were no significant differences in mean intragastric pH, MPT intragastric pH ≥3, and ≥4 between famotidine and placebo [3]. Data from 5 dogs suggest that there was already decreased control of gastric acidity on day 3 [3]. The authors advised caution when recommending long-term, daily oral administration of famotidine to dogs [3].

Cats. Sixteen healthy cats received famotidine at 0.5-1.24 mg/kg (median, 0.87 mg/kg) twice daily, or twice daily every second day, with intragastric pH recorded on treatment days 1-3 and 11-13 [4]. In the twice-daily group there was a 31% decrease in MPT intragastric pH ≥3 and a 27% decrease in MPT intragastric pH ≥4 between days 1 and 13 (P = .0007 and P = .0008 respectively), alongside a significant fall in mean intragastric pH (P = .001) [4]. Those are percentage-point changes, and the raw values make the size of the drop concrete: in the twice-daily group famotidine produced an MPT intragastric pH ≥3 of 52% and an MPT intragastric pH ≥4 of 38% on day 1, and by day 13 these had decreased to 21% and 11% respectively [4]. In the every-second-day group, no significant differences were found in mean intragastric pH (P = .90) or in MPT intragastric pH ≥3 and ≥4 (P = .84 and P = .78) on day 13 compared with day 1 [4]. Serum gastrin increased significantly with famotidine regardless of treatment frequency [4].

The more sobering point in the feline data is the starting position, not the decay. Famotidine administration did not meet the clinical acid-suppressing goals for the treatment of acid-related disorders on day 1 nor over time in the twice-daily group [4]: those goals are an intragastric pH ≥3 for 75% of the day and ≥4 for 67% of the day, against the 52% and 38% famotidine actually achieved on day 1 [4]. In cats, in other words, twice-daily famotidine did not start out adequate and then decline — it never reached the target at all.

Timing and mechanism. The consensus panel states that in dogs such tachyphylaxis occurs within 13 days and may be noticed within 3 days, and that the phenomenon appears to occur even more rapidly, within 12-72 hours, in human subjects when famotidine is administered IV [1]. Tolerance may be caused by gastrin-induced up-regulation of enterochromaffin-like cell synthesis of histamine, which in turn competes with the antagonist at the parietal cell [1].

Two things follow. First, famotidine is best understood as a short-course drug; on the canine data, a patient still on twice-daily famotidine at days 12-13 is receiving acid suppression that was not significantly different from placebo [3]. Second, the feline data raise, without settling, the possibility that every-second-day dosing preserves the effect. That was shown on intragastric pH in healthy cats, not on any clinical outcome in sick ones [4].

Evidence-based indications, and the common non-indications

Where acid suppression is genuinely warranted, famotidine is a second-line agent. PPIs are superior to H2RAs, sucralfate and misoprostol for most causes of GUE in people, and should be considered as standard of care for the medical treatment of GUE in dogs and cats [1].

The more useful half of this page is the list of situations in which famotidine is reflexively given without supporting evidence. Each of the following is a direct consensus position:

• Pancreatitis. There is no evidence that acid suppression treatment is beneficial or indicated in the management of dogs or cats with pancreatitis, unless the animal has concurrent evidence of GUE [1].
• Non-erosive gastritis. There is no evidence to support the prophylactic use of gastroprotectant therapy in dogs and cats with non-erosive gastritis. Acid suppression with famotidine at 0.5 mg/kg q24h did not affect treatment efficacy or frequency of clinical signs in 23 dogs with histologic evidence of gastritis and spiral bacteria in gastric mucosal biopsy samples [1].
• Chronic kidney disease. There is no evidence to support the prophylactic use of gastroprotectants in dogs and cats with International Renal Interest Society (IRIS) stages 1-3 renal disease, and additional studies are warranted for IRIS stage 4. In a study of 10 cats with chronic renal disease and 9 healthy age-matched control cats, no significant differences were observed in serum gastrin concentrations and gastric pH between groups, suggesting that cats with CKD may not have gastric hyperacidity compared to healthy cats and therefore may not need acid suppression [1].
• Critical illness and routine stress-ulcer prophylaxis. There is no compelling evidence that gastroprotectant therapy is beneficial or indicated in critically ill human and animal patients unless definite risk factors such as GI hemorrhage or concurrent NSAID administration are present [1].
• Hepatic disease. There is weak evidence to support the prophylactic use of acid suppressant therapy in dogs and cats with hepatic disease that is not associated with GI bleeding [1].
• Non-Helicobacter pylori Helicobacter (NHPH). There is no evidence that acid suppression treatment is beneficial or indicated in dogs or cats undergoing treatment for NHPH [1].
• Thrombocytopenia-induced bleeding. There is insufficient evidence to support the use of standard dosages of acid suppressant treatment for prevention or management of thrombocytopenia-induced bleeding [1].
• Glucocorticoid-associated ulceration after spinal surgery. In these cases there is no convincing evidence that gastroprotectant drugs are beneficial [1].

Vomiting deserves its own line, because it is the most common trigger for reaching for famotidine at all. Vomiting may be the primary sign of gastritis in dogs and cats, but acid-suppressant drugs should not be used as antiemetics [1]. A vomiting patient needs an antiemetic such as maropitant or ondansetron, not an H2RA.

Peri-anaesthetic use is a partial exception that is often misapplied. The consensus position is that there is a lack of empirical evidence in dogs and cats, but compelling evidence from studies in people, that acid-suppressing agents may be beneficial for prevention of esophagitis secondary to gastroesophageal reflux, particularly when associated with an anesthetic procedure, and that administration of PPIs does not decrease gastric reflux but may prevent injury by increasing the pH of the refluxate [1]. Crucially, the panel notes that additional studies are warranted to determine the benefits of preanesthetic administration of H2RAs in dogs and cats in which prolonged maintenance of esophageal pH > 4.0 is not necessary [1]. The studied preanesthetic protocols used PPIs. A single pre-induction dose of famotidine is not evidence-based reflux prophylaxis.

Adverse effects and cautions

Famotidine is well tolerated in dogs and cats. The reason to withhold it is usually absence of an indication, not toxicity.

Rapid IV administration in cats. The long-standing concern that IV famotidine causes hemolysis in cats has been tested directly and was not confirmed. A retrospective review of 142 hospitalized cats compared famotidine IV (n = 56), famotidine SC (n = 48) and no famotidine (n = 38) [8]. Median baseline PCVs were significantly lower in the IV (31.5%) and SC (32.0%) groups compared with the control group (35.0%; P = .04), but the median percent drop in PCV, 3-4%, was no different in cats that received famotidine by either route compared with the control group (P = .90), and no cats in either famotidine group were observed to have any clinical signs of hemolysis [8]. The authors concluded that the IV route appeared safe when famotidine was administered over 5 minutes, and that they could not document a safety advantage of SC versus IV administration in this group of cats [8]. The practical reading is to give it slowly rather than to avoid the IV route. For reference, the human injection label specifies IV injection over at least 2 minutes and IV infusion over 15 minutes to 30 minutes [5].

Renal considerations. Because these drugs are renally eliminated, dose adjustments of H2RAs based on projected glomerular filtration rate are recommended [1]. The human label quantifies the exposure change: in adult patients with severe renal impairment (creatinine clearance less than 30 mL/minute) the systemic exposure (AUC) of famotidine increased at least 5-fold, and in patients with moderate renal impairment (creatinine clearance between 30 to 60 mL/minute) the AUC increased at least 2-fold; CNS adverse reactions and QT prolongation have been reported in patients with moderate and severe renal impairment [5]. The consensus statement recommends the adjustment but does not supply a species-specific scheme [1], so the defensible approach in an azotaemic dog or cat is to lengthen the interval and use the lowest effective dose rather than to import a human milligram figure.

Drug interactions

The interaction that matters most is mechanistic and predictable: raising gastric pH reduces the absorption of drugs that require an acid environment to dissolve. The label states that famotidine can reduce the absorption of other drugs due to its effect on reducing intragastric acidity, leading to loss of efficacy of the concomitant drug [5].

In small animal practice the group to watch is the azole antifungals. Azoles such as ketoconazole, itraconazole, voriconazole and posaconazole are inherently poorly soluble, must undergo dissolution at a low pH for oral absorption, and are ideally administered orally with food to stimulate acid secretion; significant impairment of dissolution and oral absorption of ketoconazole has been shown experimentally when increasing the gastric pH profile in dogs [1]. Itraconazole solution for oral use is an exception because it is formulated in a cyclodextrin complex to maintain solubility in solution [1]. Iron is affected by the same principle, since hydrochloric acid in the stomach promotes iron absorption by reducing the ferric form to the more soluble ferrous form [1].

Do not stack famotidine on top of a PPI. There is no evidence of benefit of administration of an H2RA with a PPI for ulcer healing, and this combination may diminish the effectiveness of the PPI [1]. The effectiveness of omeprazole was markedly compromised in dogs if administered while acid secretion was inhibited by co-administration of H2RAs, and no benefit was detected in MPT intragastric pH ≥3 and 4 in healthy dogs when famotidine was administered concurrently with IV pantoprazole [1]. This follows from PPI pharmacology: PPIs need actively secreting parietal cells to bind.

One human-label interaction is worth carrying across because the co-prescription is plausible in practice: famotidine is considered a weak CYP1A2 inhibitor and, although not studied clinically, concomitant use with tizanidine should be avoided; if concomitant use is necessary, monitor for hypotension, bradycardia or excessive drowsiness [5].

Dosing considerations

Every famotidine dose in dogs and cats is extra-label [1]. The figures below are the doses actually administered in the published veterinary studies cited on this page, not label recommendations, and they are reported so you can see what the evidence was generated on.

• Dogs, oral. 1.0-1.3 mg/kg q12h in the crossover study that produced MPT at pH ≥3 of 22 ± 8% [2]; 1.0 mg/kg q12h for 14 consecutive days in the tachyphylaxis study [3].
• Dogs, IV intermittent. 0.5 mg/kg IV q12h significantly suppressed gastric acid secretion versus saline solution in healthy Beagles, and 0.5 mg/kg IV q8h was evaluated separately in 6 dogs [6]. A different study used 1.0 mg/kg IV q12h as its intermittent comparator [7].
• Dogs, IV constant-rate infusion. 1.0 mg/kg IV loading bolus followed by 8.0 mg/kg/day continuous infusion, studied over 3 consecutive days [7].
• Cats, oral. 0.5-1.24 mg/kg (median, 0.87 mg/kg) twice daily, or the same dose twice daily every second day, over 14 days [4]. The consensus statement separately cites 0.88-1.26 mg/kg PO q12h as significantly more efficacious than placebo but inferior to omeprazole in healthy colony cats [1].

Two rules of thumb follow from the evidence rather than from custom. Frequency beats milligrams: there is a lack of benefit for once-daily H2RA administration in dogs and cats for GUE and reflux esophagitis [1], so if famotidine is worth giving it is worth giving at least twice daily. And duration beats both: plan a short course with a defined endpoint, because the pH effect is already measurably reduced by days 12-13 in dogs [3] and by day 13 in cats [4].

Monitoring

There is no bedside assay for acid suppression, so monitoring is clinical. Define the endpoint before you start (resolution of melena or haematemesis, healing of an endoscopically documented lesion) and set a review date rather than an open-ended repeat.

Two facts should shape expectations. The degree of gastric acid suppression necessary for GUE prophylaxis or treatment in dogs and cats is undetermined [1], so pH targets used in these studies are borrowed from human medicine rather than validated in either species. And if a patient with GUE is not improving, escalating the famotidine dose is the wrong lever, since higher dosages of famotidine (1-1.3 mg/kg q12h) had only a weak effect on intragastric pH in healthy dogs [1]. Switch class instead.

The consensus statement supplies a taper protocol only for PPIs: the consensus opinion is that PPIs should be tapered in dogs and cats after prolonged use of more than 3-4 weeks [1]. It gives no equivalent famotidine protocol, though rebound acid hypersecretion after abrupt H2RA withdrawal is described in humans as a consequence of the same gastrin-driven tolerance [1].

When a PPI is the better choice, and when neither is indicated

Choose a PPI when the goal is genuine, sustained acid suppression: documented or strongly suspected GUE, erosive or reflux esophagitis, NSAID- or neoplasia-associated ulceration, or oesophageal mucosal protection in a high-risk anaesthetic candidate. Based on evidence from studies in humans and research animals, PPIs administered twice daily are superior to other gastroprotectants for treating acid-related GUE [1], and the canine pH data show how large that difference is in practice [2]. Dosing, formulation and taper detail sit in the companion hub on omeprazole and gastroprotectants.

Famotidine still has a defensible niche. A short course of days rather than weeks, where a modest and immediate reduction in acid is wanted and the delayed onset of a PPI is a real disadvantage; patients in whom an oral PPI is impractical or not tolerated; and the injectable setting, where a CRI reached acid-suppression targets that intermittent dosing did not [7].

Choose neither when there is no acid-related lesion to treat, which covers a large share of real prescriptions: uncomplicated pancreatitis, non-erosive gastritis, IRIS stage 1-3 CKD, hepatic disease without GI bleeding, and routine ICU prophylaxis in a patient with no GI hemorrhage and no concurrent NSAID [1]. As of August 2026 the most recent published overview of acid-suppressant use across human and veterinary medicine is a 2024 One Health review, which describes rising overuse of these drugs in dogs and cats alongside a need for expanded feline research and better understanding of which diseases benefit from gastroprotection [9]. Stopping an unnecessary famotidine is a clinical decision in its own right, not an omission.

Frequently Asked Questions

Is famotidine as effective as omeprazole in dogs? No. In a randomized 4-way crossover study in six healthy dogs, oral famotidine at 1.0-1.3 mg/kg q12h held intragastric pH ≥3 for 22 ± 8% of the time, compared with 63 ± 14% for an omeprazole tablet at 1.5-2.6 mg/kg q24h. The 2018 ACVIM consensus statement concludes that H2RA monotherapy given twice daily is inferior to twice-daily PPI treatment, and that PPIs should be considered standard of care for the medical treatment of gastroduodenal ulceration and erosion in dogs and cats.

How quickly does famotidine tachyphylaxis develop, and is it real in cats too? It is real in both species. In dogs given 1.0 mg/kg q12h orally for 14 days, mean pH fell by 1.63 and mean percent time at pH ≥3 and ≥4 fell by 33 and 45% on days 12-13 compared with days 1-2 — by which point there were no significant differences in acid suppression between famotidine and placebo, and data from 5 dogs suggested decreased control of gastric acidity as early as day 3. In cats given a median of 0.87 mg/kg twice daily, mean percent time at pH ≥3 fell from 52% on day 1 to 21% by day 13, and at pH ≥4 from 38% to 11%. The ACVIM consensus statement notes that in dogs tachyphylaxis occurs within 13 days and may be noticed within 3 days, and that in humans it appears within 12-72 hours when famotidine is given IV.

Does every-other-day dosing avoid tolerance in cats? On intragastric pH, it appears to. Cats dosed twice daily every second day showed no significant differences in mean intragastric pH (P = .90) or in mean percent time at pH ≥3 and ≥4 (P = .84 and P = .78) on day 13 versus day 1, while the every-day group deteriorated significantly. Serum gastrin rose with famotidine regardless of frequency. Two caveats matter. Famotidine did not meet the clinical acid-suppressing goals in the every-day group on day 1 either, so preserved is not the same as adequate. And this was a healthy-cat pH study, not a clinical outcome trial, so treat intermittent dosing as biologically plausible rather than proven to help sick patients.

Should I prescribe famotidine for pancreatitis? Not by default. The 2018 ACVIM consensus statement is explicit that there is no evidence that acid suppression treatment is beneficial or indicated in the management of dogs or cats with pancreatitis, unless the animal has concurrent evidence of gastroduodenal ulceration or erosion. The rationale usually offered, an increased risk of upper GI bleeding, rests on an incidence in dogs and cats with pancreatitis that is currently unknown. Treat pain, fluid deficits and nausea on their own merits instead.

Is intravenous famotidine safe in cats? The hemolysis concern has been tested and not confirmed. A retrospective review of 142 hospitalized cats found the median percent drop in PCV (3-4%) was no different in cats receiving famotidine IV (n = 56) or SC (n = 48) compared with controls (n = 38), P = .90, and no cat in either famotidine group showed clinical signs of hemolysis. The authors concluded the IV route appeared safe when famotidine was administered over 5 minutes and that they could not document a safety advantage of SC over IV. Give it slowly; the human injection label specifies IV injection over at least 2 minutes.

Can I combine famotidine with omeprazole for additive acid suppression? No, and it may be counterproductive. The ACVIM consensus statement states there is no evidence of benefit of administering an H2RA with a PPI for ulcer healing, and that this combination may diminish the effectiveness of the PPI. The effectiveness of omeprazole was markedly compromised in dogs when given while acid secretion was already inhibited by an H2RA, and no benefit was detected in mean percent time at pH ≥3 and 4 in healthy dogs when famotidine was given concurrently with IV pantoprazole. PPIs need actively secreting parietal cells in order to bind.

Does famotidine need a dose reduction in chronic kidney disease? Adjustment is recommended in principle. The ACVIM consensus statement advises dose adjustments of H2RAs based on projected glomerular filtration rate because of their renal elimination, but supplies no species-specific scheme. The human label reports that in severe renal impairment (creatinine clearance less than 30 mL/minute) famotidine AUC increased at least 5-fold, and in moderate impairment (30 to 60 mL/minute) at least 2-fold, with CNS adverse reactions and QT prolongation reported in these patients. The prior question, though, is whether acid suppression is indicated at all: there is no evidence supporting prophylactic gastroprotectants in IRIS stages 1-3.

Is famotidine an antiemetic? No. The ACVIM consensus statement states directly that although vomiting may be the primary sign of gastritis in dogs and cats, acid-suppressant drugs should not be used as antiemetics. Famotidine reduces gastric acid secretion; it has no action at the emetic centre or the chemoreceptor trigger zone. A vomiting patient needs a drug matched to the mechanism, such as maropitant or ondansetron, and a diagnostic plan for the underlying cause.