Antihistamines Three types of histaminergic receptors 





Selective agonists

2-Methyl histamine


2-Thiazolyl ethylamine



α- methyl histamine


Selective antagonist








Receptor type

Gq-protein coupled

Gs- protein coupled

Gi/Go protein coupled

Effector pathway

PIP2 hydrolysis – IP3/DAG: release of Ca2+ from intracellular stores

Protein kinase C activation

NO release – cGMP

Adenylyl cyclase activation – cAMP increase – phosphorylation of specific proteins

Restricting Ca2+ influx

K+ channel activation

cAMP decrease

Distribution in the body:

Action mediated

Smooth muscle contraction

Blood vessels: vasoconstriction, increase capillary permeability

Stimulation of afferent nerve endings

Ganglionic cell stimulation

Release of CAs in adrenal medulla

Brain: transmitter

Gastric glands: acid secretion

Blood vessels: vasodilatation

Heart: + chronotropy,

+ ionotropy

Uterus: relaxation

Brain: transmitter

Brain: inhibition of histamine release – sedation

Lung, spleen, skin, gastric mucosa- decrease histamine release


 Clinical classification of antihistaminics Highly sedative

  • Diphenhydramine : 25-50 mg oral
  • Dimenhydrinate: 25-50 mg oral
  • Promethazine: 25-50 mg oral, im
  • Hydroxyzine: 25-50 mg oral, im

 Moderately sedative

  • Pheniramine: 25-50 mg oral, im
  • Cyproheptadine: 4 mg oral
  • Meclozine (Meclizine): 25-50 mg oral
  • Cinnarizine: 25-50 mg oral

 Mild sedative

  • Chlorpheniramine: 2-4 mg (0.1 mg/kg) oral, im
  • Dexchlorpheniramine: 2 mg oral
  • Triprolidine: 2.5-5 mg oral
  • Clemastine: 1-2 mg oral

 Second generation anti histaminics

  • Fexofenadine: 120-180 mg oral
  • Loratadine: 10 mg oral
  • Desloratadine: 5 mg oral
  • Cetirizine: 10 mg oral
  • Levocetirizine: 5-10 mg oral
  • Azelastine: 4 mg oral, 0.28 mg intranasal
  • Mizolastine: 10 mg oral
  • Ebastine: 10 mg oral
  • Rupatadine: 10 mg oral

   Pharmacological actions 

1. Antagonism of histamine

  • They effectively block histamine induced bronchoconstriction, contraction of intestinal and other smooth muscle and triple response- especially wheal, flare and itch
  • Fall in BP produced by low doses of histamine is blocked
  • Release of adrenaline from adrenal medulla in response to histamine is abolished
  • Action of histamine on gastric secretion is not affected by these drugs
  • Cyproheptadine has additional 5-HT2 receptor blocking activity

 2. Antiallergic action

  • Many manifestation of immediate hypersensitivity (type 1 reaction) are suppressed
  • Urticaria, itching and angioedema are well controlled
  • Anaphylactic fall in BP is only partially prevented
  • Asthma is practically unaffected.

 3. CNS 

  • Causes variable degree of CNS depression. It depends on the ability of the compound to cross the blood brain barrier and  its affinity for the central H1 receptors
  • Also causes sedation. 2nd generation antihistaminics are practically non sedating
  • Excitement and convulsions are frequently seen in toxic doses
  • Certain antihistamines are effective in preventing motion sickness. They are also effective to control vomiting of pregnancy and other causes
  • Promethazine and few other antihistaminics also reduce tremor, rigidity and sialorrhea of parkinsonism
  • Some antihistaminics like cyproheptadine have appetite stimulating effect
  • Some antihistamines are also effective antitussives

 4. Anti cholinergic actions 

HighLowMinimal/ absent

  5. Local anesthetic

  • Some drugs like pheniramine, promethazine, diphenhydramine have strong while others have weak membrane stabilizing property
  • Membrane stabilizing property also confers antiarrhythmic property to these compounds

 6. BP

  • Most antihistamines cause a fall in BP on iv injection (direct smooth muscle relaxation or α adrenergic blockade as in promethazine)


  • Conventional H1 antihistamines are well absorbed from oral and parental routes, metabolized in the liver and excreted in urine
  • They are widely distributed in the body and enters brain
  • The newer compounds penetrate brain poorly accounting for low or absent sedative action
  • Duration of action of most agents is 4-6 hours except for meclozine, chlorpheniramine, mesolastine, loratidine, cetirizine and fexofenadine which act for 12-24 hours or more

Side effects and toxicity

  • Sedation
  • Diminished alertness and concentration
  • Light headedness
  • Motor incoordination
  • Fatigue
  • Tendendency to fall asleep
  • Impairment of psychomotor performance
  • Regular use in children causes CNS depression which may interfere with learning and academic tasks
  • Anticholinergic effects like dryness of mouth, alteration of bowel movement, urinary hesitance and blurring of vision
  • Epigastric distress and headache
  • Local application causes contact dermatitis

Acute overdosage causes following symptoms:

  • Central excitation
  • Tremors
  • Hallucinations
  • Muscular incoordination
  • Convulsions
  • Flushing
  • Hypotension
  • Fever
  • Death due to respiratory or cardiovascular failure

 Second generation antihistaminics​They have following properties:

  • Absence of CNS depressant property
  • Higher H1 selectivity, no anti cholinergic side effects
  • Additional anti allergic mechanisms apart from histamine  blockade
  • Does not impair psychomotor performance
  • Produce no sedation, do not potentiate alcohol or benzodiazepines
  • Their principal indications are:Allergic rhinitis and conjunctivitis, hay fever, pollinosis- control sneezing, runny but not blocked nose, and red watering itchy eyes; Urticaria, dermographism, atopic eczema; Acute allergic reactions to drugs and food
  • They have poor antipruritic, antiemetic and antitussive actions

Uses 1. Allergic disorders

  • Itching, urticaria
  • Seasonal hay fever
  • Allergic conjunctivitis
  • Angioedema of lips
  • Not effective in bronchial asthma due to following reasons:

i. Leukotrienes (C4, D4) and PAF are more important mediators than histamine

ii. Concentration of antihistamines attained at the site may not be sufficient to block high concentration of histamine released locally in the bronchi

  • Type 1 hypersensitivity reactions to drugs (except asthma and anaphylaxis) are suppressed

2. Other conditions involving histamine

  • Insect bite
  • Ivy poisoning
  • Abnormal demographism are suppressed

3. Pruritides

4. Common cold

5. Motion sickness

6. Vertigo

7. Pre anesthetic medication

8. Cough

9. Parkinsonism

10. Acute muscle dystonia

11. As sedative, hypnotic, anxiolytic  Diphenhydramine 

  • Injectable 1% diphenhydramine is a safe, inexpensive and effective local anesthetic for simple dermatological procedured in patients with caine allergies. (1)
  • Diphenhydramine may not be an effective sedative/hypnotic in elderly women. (2)
  • Diphenhydramine and dextromethorphan are not effective in providing nocturnal symptom relief for children with cough and sleep difficulty. (3)
  • The valerian-hops combination and diphenhydramine may be a useful adjunts in the treatment of mild insomnia. (4)
  • Opsoclonus occurs due to diphenhydramine poisoning. (5)
  • The sedative effect of diphenhydramine might be caused by coadministration of CYP2D6 sustrates/ inhibitors. The large differences in the metabolic activities of CYP2D6 and those of CYP1A2, CYP2C9 and CYP2C19 could cause the individual differences in anti-allergy efficacy and the sedative effect of diphenhydramine. (6)
  • Haloperidol abuse can be treated with diphenhydramine. (7)
  • Life threatening diphenhydramine overdose can be treated with charcoal hemoperfusion and hemodialysis. (8)
  • Diphenhydramine is less potent than bupivacaine at producing cutaneous analgesia. At equipotent doses for infiltrative cutaneous analgesia, the duration of action of diphenhydramine is equal to that of bupivacaine. (9)
  • Diphenhydramine may be useful as a palliative treatment for patients dying with Parkinson’s disease and tremors. (10)
  • Metoclopramide administered with diphenhydramine (MAD) regimen is effective for the treatment of headaches in pregnant women when acetaminophen alone is ineffective, using codeine as standard for comparison. (11)
  • Topical diphenhydramine may be a safe alternative in patients requiring topical ocular anesthesia who have multiple allergies to topical anesthetics. (12)
  • Hyponatermia and obstructive uropathy can be induced by the antihistamine diphenhydramine in patient with no psychiatruc history. (13)


  • Oral dimenhydrinate does not significantly decrease the frequency of vomiting in children with acute gastroenetritis. (14)
  • Dimenhydrinate and betahistine should not be used together because of their opposite effects on the vestibular system. Dimenhydrinate can be used to treat acute episode of vertigo. (15)
  • A lower rate of obstructive uropathy is found in infants born to mothers treated with dimenhydrinate during the first trimester of pregnancy than in infants whose mothers did not take the drug at that time. (16)
  • Intramuscularly administered dimenhydrinate seemed to reduce postoperative vomiting in patients. (17)
  • Rectal administration of dimenhydrinate is an effective means of reducing postoperative vomiting in children undergoing strasbismus surgery. (18)
  • Overdose with dimenhydrinate and diphenhydramine, both of which are over-the-counter drugs, can result in rapid central nervous system stimulation, including status epilepticus. Death can occur within two hours. (19)
  • Erythema multiforme can occur secondary to dimenhydrinate in a patient with previous similar reactions to pamabrom. (20)
  • Fixed drug eruptions can be caused by dimenhydrinate. (21)
  • The antimotion sickness property of diphenhydramine and dimenhydrinate may be due to diminished excitability of the vestibular nuclear complex. (22)
  • Prophylactic dimenhydrinate in a dose of 50 mg effectively decreases the incidence of emesis  without any increase in side effects following cesarean delivery with intrathecal morphine. (23)
  • Clozapine helps to reduce carvings for dimenhydrinate. (24)
  • Dimenhydrinate degrades night-vision, reaction time and stereopsis in patients. (25)
  • Intra-operative dimenhydrinate followed by three further administrations after surgery, reduces the incidence and the severity of postoperative nausea and vomiting without side effects. (26)
  • The use of dimenhydrinate in children with vomiting is associated with a risk of delay in the diagnosis of treatable medical conditions. (27)
  • The fixed low dose combination of cinnarizine 20 mg + dimenhydrinate 40 mg is effective, clinically beneficial and well tolerated in patients with vestibular vertigo of central and/ or peripheral origin. (28)
  • Lansoprazole, clonazepam and dimenhydrinate is capable of attenuating the symptoms of patients with intractable hiccups. (29)
  • Dimenhydrinate augments heart rate responses to baroreceptor unloading, but does not alter resting muscle sympathetic nerve activity (MSNA), the sympathetic baroreflexes or the vestibulosympathetic reflex. (30)


  • Intravenous promethazine administration results in serious tissue injury like burning, erythema, pain, swelling, severe spasm of vessels, thrombophlebitis, venous thrombosis, nerve damage, paralysis, abscess, tissue necrosis and gangrene. (31)
  • Promethazine potentiates the action of different narcotics like morphine, pethidine, oxymorphine, hydromorphone, fentanyl and pentazocine. (32)
  • Promethazine is not recommended as a first line agent in the treatment of post operative nausea and vomiting, but can be considered for use as a rescue antiemetic. (33)
  • Physiostigmine is used in the treatment of promethazine poisoning. (34)
  • Phenothiazine has a potent sedative action, marked antiemetic effect, and has synergism with narcotocs, barbiturates and anesthetic agents. Induction and maintenance of general anesthesia is facilitated by promethazine. It should not be used in patients with a history of preeclampsia, epilepsy, convulsions, intracranial trauma and severe hypertension. (35)
  • Haloperidol plus promethazine is effective in the management of psychosis induced aggresion. (36)
  • Depression can be treated with combination of chlorpromazine and promethazine. (37)
  • Topical promethazine can cause contact dermatitis, inflammmation and photosensitivity. It may cause acute or chronic urticaria, eczema, pruritis, papular rash or erythema, fixed drug eruptions (FDE). (38)
  • The intranasal microsphere formulation of promethazine offers great promise as an effective non-invasive alternative for treating space motion sickness due to its rapid absorption and bioavailability equivalent to the im dose. (39)
  • Promethazine is reported to cause significant sedation, agitation, hallucinations, seizures, dystonic reactions and apparent life threatening evets or sudden infant death syndrome. It should be used only for appropriate indications and only in children greater than 2 years of age. (40)
  • Promethazine works significantly better than promethazine for relieving symptoms of nausea and vomiting more quickly and completely in ED patients withuncomplicated nausea and vomiting. (41)
  • Promethazine appers to have less sedative and peripheral vasodilator effects than acepromazine, thus it could be safer than acepromazine in patients suffering from hypotension. (42)
  • Pretreatment with rpomethazine significantly decreases mivacurium induced histamine release in children and provide stable hemodynamics during administration of anesthesia. (43)


  • Hydroxyzine apperas to be safe and effective in adults with generalized anxiety disorder. (44)
  • The incidence of bone pain with Granulocyte-Colony Stimulating Factor (G-CSF) may be higher clinically than reported before. Hydroxyzine is effective to the bone pain, and it also protects against the onset of the bone pain. (45)
  • Hydroxyzine 25 mg at bed time improves sleep behaviour in patients with cirrhosis and minimal hepatic encephalopathy (HE). The risk of precipitating over HE warrants some caution when prescribing this drug. (46)
  • The anxiolytic effects of chloral hydrate and hydroxyzine are not additive or synergistic. (47)
  • Hydroxyzine 0.7 mg/kg three timed daily is as effective as hydroxyzine 1.4 mg/kg three times daily in relieving pruritis and promoting resolution of the skin lesions in children with atopic dermatitis. The 0.7 mg/kg tid dose causes significantly less sedation than the 1.4 mg/kg tid dose. (48)
  • The addition of hydroxyzine to ephedrine may enhance its antiemetic efficacy. The combination may offer a more suitable alternative to droperidol or ephedrine alone in the outpatient setting. (49)
  • Hydroxyzine and benztropin selectively inhibits hepatitis C virus infection. They inhibit viral entry at a post-binding step of geotypes 1,2,3 and 4 without affecting entry of other viruses. (50)
  • Hydroxyzine has a tranquillizing effect but is not sufficient for treatment of psychotic conditions. It may be effective in minor disturbances like neuroses. (51)
  • Hydroxyzine may be used in the treatment of restless leg syndrome. (52)
  • Hydroxyzine, 25 mg to 100 mg nightly, seems to be effective in adults and geriatric patients and it is more rational choice in patients with insomnia. (53)
  • Hydroxyzine is clinically effective in the treatment of acute arrhythmias particularly ventricular premature beats, paroxysmal tachycardias, ventricular extrasystoles complicating atrial fibrillation. (54)
  • Hydroxyzine 1-2 mg/kg after an appropriate premedication-interval provides no better anxiolysis than placebo in the pre-operative period. (55)
  • First generation H1 blockers are not associated with an increased risk of major malformations or any other adverse fetal effects when given to a pregnant women. Second generation H1 blockers have also not been associated with an increased risk of adverse pregnancy outcomes. None of the antihistamines is excreted in the breast milk in an appreciable amount so as to have any adverse effects on breastfeeding infant. (56)


  • Acute renal failure can be caused by pheniramine maleate induced rhabdomyolysis. (57)
  • Prophylactic pheniramine/ naphazoline are more effective than olopatadine and plcebo in alleviating the signs and symptoms of acute ocular allergic reaction. (58)
  • Pheniramine overdisage can lead to central anticholinergic syndrome with choreiform movements. (59)
  • Pheniramine has a protective effect against ischemic/ reperfusion injury in rat lung. (60)
  • Therapeutic levels of pheniramine after taking 75 mg pheniramine maleate vary from 0.01 to 0.19 µg/ml of blood. (61)
  • A comparison of the urinary excretion data of pheniramine and its halogenated derivatives indicate the compounds to be metabolized in the following order: pheniramine < chlorpheniramine < brompheniramine. This is inverse to the order of total free and N-demethylated drug excreted in the urine. (62)
  • Loratidine is found to be more effective than pheniramine maleate in chronic idiopathic urticaria. (63)
  • There is occurence of psychotic syndromes with heavy pheniramine use. The psychopathology can vary from an independent psychotic syndrome to an organic brain syndrome like disorder. (64)
  • The metabolism of phenirmaine maletae can be impaired in Gilbert syndrome and anticholinergic effects can cause accomodation paralysis. (65)


  • Cyproheptadine inhibits growth hormone and ACTH secretion during sleep in man probably by antagonizing serotonergic mechanisms. (66)
  • Patients receiving cyproheptadine show marked increase in appetite, an associated weight gain and accleerated linear growth rate. (67)
  • There is a significant weight gain, increase in subjective hunger ratings and food intake with cyproheptadine. Drowsiness is the most frquent side effect. (68)
  • Cyproheptadine may be useful adjunct to baclofen and benzodiazepines in the management of acute intrathecal baclofen withdrawal syndrome. (69)
  • Cyproheptadine act as an appetite stimulant at a dose which appear to have antiserotoninergic activity. Administered orally for upto 6 oestrous cycles, it does not affect 24h food intake. It reduces 24h liquid intake and 24h urine output. (70)
  • Cyproheptadine may be effective as a migraine-preventive treatment for patients in whom conventional drugs have been ineffective or have caused side effects. (71)
  • Cyproheptadine can reduce spasticity and enhance locomotor function in spinal cord injured patients. (72)
  • The ability of cyproheptadine to antagonize the intestinal effects of methadone suggests a potentially useful means of overcoming one of the most troublesome side effects of the narcotic drugs. (73)
  • Cyprohepatdine suppresses the PI3K/AKT signalling pathway, which is probably critical for cyproheptadine induced myeloma cell apoptosis. It displays anti-blood cancer activity. (74)
  • Cyproheptadine and citalopram can cause fatality. (75)
  • The combination of cyproheptadine and propanolol is effective in migraine prophylaxis. (76)
  • Use of cyproheptadine in cystic fibrosis patients shows a significant weight gain and increase in BMI after 12 weeks. It can be an alternative approach for patients who need nutritional support for a short period of time. (77)
  • Cyproheptadine may be safe, rapidly effective treatment of serotonin syndrome. Physicians should be aware of its anticholinergic effects like urinary retention which may be potentiated by monoamine oxidase inhibitors. (78)
  • Cyproheptadine is safe and effective for treating dyspeptic symptoms in children, particularly in young children and those with early vomiting and retching after fundoplication. (79)
  • The primary action of cyproheptadine in preventing contractions of the canine basilar artery is antagonism of calcium channels. Thus it can be used for migraine prophylaxis and in the treatment of headache and other neurological disorders. (80)
  • Cyproheptadine may be effective in post traumatic stress disorder (PTSD) nightmare treatment. (81)
  • Cyproheptadine may be useful in neuroleptic- induced akathisia. (82)


  • Meclizine attentuates mitochondrial respiration by directly inhibiting the Kennedy pathway of phosphatidylethanolamine biosynthesis. (83)
  • Meclizine hold therapeutic potential in the treatment of polyQ toxicity disorderd such as Huntington’s disease. (84)
  • Meclizine is effective for preventing nausea and vomiting associated with Yuzpe regimen of emergency contraceptive pills. Women using this drug should be cautioned to anticipate drowsiness. (85)
  • Meclizine reduces the severity and frequency of attacks as well as signs and symptoms associated with vertigo including nausea, positional and positioning nystagmus and postural instability. (86)
  • Meclizine ehnaces sensorimotor gating in healthy male subjects with high startle responses and low prepulse inhibition. (87)
  • Meclizine does not act as a human constitutive androstane receptor (hCAR) inverse agonist or antagonist in human hepatocytes. Therefore, it is not appropriate to use this drug as a pharmacological tool to study hCAR function in this cell type. (88)
  • Meclizine is effective for the prevention and treatment of motion sickness, particularly dring mild civilian travel. It is well tolerated with few adverse efefcts. Its oral dosage form is convineient for patients to take prior to exposure to motion as a preventative measure. (89)
  • Meclizine hydrochloride-niacin combination is found to be very useful for treatment of ambulatory patients with vestibular disease. (90)


  • Cinnarizine is safe and effective in reducing both headache and vertigo aspects of migraine plus vertigo among the patients who suffer from either vestibular migraine or migraine with brainstem aura associated with vertigo. (91)
  • Betahistine has better effect on symptom reduction in patients with Meniere’s disease compared to cinnarizine. (92)
  • Cinnarizine can be used for prophylaxis of car sickness in childre. (93)
  • Cinnarizine aggravates the symptoms of Parkinson’s disease. (94)
  • Cinnarizine is an efficacious and well tolerated prophylactic antimigraine medication which has early onset effectiveness. (95)
  • Cinnarizine and flunarizine have a potential risk to induce extrapyramidal reactions and depression. (96)
  • Cinnarizine has an antagonist effect on dopamine D2 receptors, has a potential antipsychotic effect with an atypical profile which should be evaluated clinically. (97)
  • Pediatric patients with cinnarizine overdose need to be observed in a health care facility for potential neurologic complications (alterations in consciousness, stupor, coma, vomiting, extrapyramidal symptoms, convulsions and hypotonia) and be treated symptomatically. The delay to onset of clinical effect should be considered in the observation period. (98)
  • Cinnarizine and betahistine is used in the treatment of vertigo and meniere’s disease. (99)
  • Cinnarizine could well prove to be the first of a new family of anti-asthmatic drugs pffering a protective effect when taken systematically. (100)
  • Cinnarizine impoves the haloperidol induced brain oxidative stress and impairment of learning and memory in the water maze test in mice. (101)
  • Flunarizine and cinnarizine induced parkinsonism is a recognized condition with specific clinical features and is the second most common cause of parkinsonism in many countries. (102)
  • A neuroleptic like action of flunarizine and cinnarizine seems to be the major reason for their extra-pyramidal side effects. Older age and long term treatment are predisposing factors of these effects. (103)
  • Chronic treatment with cinnarizine alters both D1 and D2 receptor densities, with a higher sensitivity of the D1 subtype. This indicates that the interactions between dopamine recpetor subtypes may be necessary for the full expression of behavioural event mediated by the D2 receptors. (104)
  • A patient with angioedema with C1 esterase inhibitor deficiency responds well to cinnarizine and alcohol abstinence. (105)


  • Chlorpheniramine/ paracetamol combination may be useful as a medication for colds in hypertensive patients since it does not induce cardiovascular effects such as those observed with pseudoephedrine. (106)
  • Chlorpheniramine analogues reverse chloroquine resistance in plasmodium falciparum by inhibiting PfCRT. (107)
  • Parallel infusion of hydrocortisone ± chlorpheniramine bolus injection to prevent acute adverse reactions to antivenom for snakebites. (108)
  • Chlorpheniramine is an effective treatment on anxiety and emotional memory in mice. (109)
  • Terfenadine and chlorpheniramine maleate is effective in the treatment of perennial rhinitis. (110)
  • Chlorpheniramine is a safe, non-cardiotoxic and well tolerated antidepressant. (111)
  • Chlorpheniramine plasma concentrations do not predict H1 receptor antagonist in plasma. There is a role of CYP2D6 in formation of a potent active metabolite of chlorpheniramine. (112)
  • Intentional overdose of lamotrigine, chlorpheniramine and citalopram causes reduced level of consciousness and ECG abnormalities, a widened QRS and a prolonged corrected QT (QTc) interval. Prompt treatment with early intubation, along with magnesium for cardioprotection and administration of sodium bicarbonate leads to quick recovery with a short intensive care stay and good outcome. (113)
  • Chlorpheniramine maleate may be a good candidate as an add-on therapy for epilepsy. (114)
  • Chlorpheniramine impairs the consolidation of learning both on telencephalon ablated animals and in sham operated ones through its action on mesencephalic structures of the brain and/ or on the cerebellum in teleost fish. (115)
  • There is an interaction of phenytoin with chlorpheniramine. (116)
  • Levamisole and chlorpheniramine maleate combination is found to more effective than antihistamine alone in the treatment of patient with urticaria. (117)
  • Chlorphenimramine is a widely used drug for managemnt of allergic reaction. The serious adverse reaction is extremely rare. A case has been reported of acute anaphylactic reaction due to expired chlorpheniramine injection. (118)
  • A fixed dose combination of paracetamol, chlorpheniramine and phenylephrine is safe and effective symptomatic treatment of the common cold or flu-like syndrome in adults. (119)
  • Cetrizine given once daily or in divided doses twice daily and chlorpheniramine given 3 times daily are effective in the treatment of seasonal allergic rhinitis in children aged 6-11 years. It has a rapid onset and is not associated with worsening of asthma. (120)


  • The fraction of the dose of triprolidine excreted in breast milk is estimated to be 0.06-0.2% in nursing mothers. (121) 
  • Hallucination has been reported in a child after drinking triprolidine/ pseudoephedrine linctus. (122)
  • The absolute oral bioavailability of triprolidine in the dog is low. There is similarity in the elimination characteristics of triprolidine in dogs, rabbits, rats and humans. (123)
  • Pseudoephedrine alone or in combination with triprolidine is effective in the treatment of common cold symptoms like sneezing, nasal obstruction etc. (124) 
  • The plasticizer and penetration enhancer increase the skin penetration of triprolidine and the triprolidine-EVA matrix system could be developed as a transdermal delivery system providing the increased constant plasma concentration and antihistamine effects. (125)
  • Under oxidative stress conditions, triprolidine undergoes distint biotransformation to give two degradation products: Triprolidine N-Oxide and Pyridin-2-yl-p-tolyl-methanone. (126)
  • Triprolidine 10 mg causes impairment of psychomotor and cognitive function in an individual while ebastine in a dose of 10-20 mg is free from impairment of psychomotor and cognitive function. (127)


  • Clemastine is a useful antipruritic agent in the cats. (128)
  • Clemastine, a specific H1 receptor antagonist is an effective broncholdilator. (129)
  • Clemastine is effectibe in the management of allergic pruritis in dogs. (130)
  • Clemastine fumarate is effective in the treatment of rhinorrhea and sneezing associated with the common cold. (131)
  • Clemastine might be of use in the treatment of acute reactions to aspirin. (132)
  • Inhalation of 0.6 mg clemastine provides significant protection against histamine induced bronchoconstriction in normal and asthmatic patients is comparable to intravenous administration of 1.0 mg clemastine. In normal subjects 2.0 mg clemastine orally was significantly less effective than iv and inhalational routes whereas in asthmatics n enhanced reaction to histamine is observed. (133)
  • Both c-Myc and STAT transcription factors are highly expressed in proliferating tumours, whgich are inhibited by clemastibe, desloratidne. Thus, they could complement established chemotherapies for cutaneous T-cell lymphomas and other cancers. (134)
  • Drowsiness can occur due to clemastine transmitted in breast milk. (135)
  • Clemastine is a high potency inhibitor of the HERG K+ channel. (136)
  • The antihistamine drug clemastine does not abolish the potentiation, which suggest that the effect of PGE1 on itch does not depend on the liberation of endogenous histamine. (137)
  • Clemastine is not appropriate for oral administration due to low bioavailability. When using repeated iv administration, the drug has to be administered atleast three to four times daily to maintain therapeutic plasma concentrations because of the short half life. If sufficient plasma concentrations is maintained, the drug is efficacious in reducing histamine induced wheal formation. (138)
  • Clemastine causes immune suppression through inhibition of extracellular signal-regulated kinase-dependent proinflammatory cytokines. (139)
  • Clemastine is the first choice antihistamine as well as an effective alternative where tolerance to other antihistamines develops in the treatment of hay fever. (140)
  • Ketotifen has antihistaminic actions in man equivalent in potency to clemastine but does not appear to have additional effects on immediate skin or bronchial responses to allergen in atopic patients. (141)
  • Low dose clemastine provides relief for sneezing and rhinorrhea and might be useful in the treatment of allergic rhinitis. (142)


  • In a skin test model of wheal and flare suppression, fexofenadine shows rapid distribution into the skin compartment with faster onset of action and greater potency vs loratidine. (143)
  • Fexofenadine at doses up to 180 mg appears free from disruptive effects on aspects of psychomotor and cognitive function. (144)
  • The antihistamine fexofenadine does not affect IKr currents in case of drug induced arrhythmia. (145)
  • Fexofenadine demonstrates no antitussive activity against capsaicin-induced cough in healthy volunteers and subjects with URI. This reflects the lack of anticholinergic activity and central nervous penetrance that is characteristic of forst generation antihistamines. (146)
  • Fexofenadine HCl at doses of 180 mg and 240 mg once daily is effective and well tolerated in the treatment of chronic idiopathic urticaria. (147)
  • Fexofenadine-pseudoephedrine and loratidine-montelukast have comparable efficacy in improving symptoms, Rhinoconjunctivitis Quality of life questionnaire (RQLQ) scores and nasal obstruction in seasonal allergic rhinitis. (148)
  • Fexofenadine is effective for the treatment of allergic rhinitis and chronic idiopathic urticaria. (149)
  • Although central nervous system (CNS) activation occurs after fexofenadine treatment, the magnitude of the centrally activating effects is too small to produce relevant performance improvement at the behavioural level. (150)
  • Patients who are dissatisfied with loratidine reports equal or better satisfaction with desloratidine as fexofenadine. Patients with severe allergic rhinitis reports greater satisfaction when converted from loratidine to desloratidine than fexofenadine. (151)
  • Fexofenadine HCl 180 mg has a faster onset of action at suppressing histamine induced flare and provides greater overall flare and wheal suppression than desloratidine 5 mg. (152)
  • QT lengthening and arrhythmias are seen in patients treated with fexofenadine. (153)
  • Desloratodine, fexofenadine and levocetrizine are appropriate options for the treatment of nasal congestion in patients with allergic rhinitis. (154)
  • The combination therapy of fexofenadine and montelukast is effective in patients with conventional therapy resistant prurigo nodularis and pemphigoid nodularis. (155)
  • Fexofenadine HCl at a single daily dose of 180 mg is an effective nonsedating antihistamine for the treatment of chronic idiopathic urticaria and is devoid of any significant adverse effect including cardiotoxicity. (156)
  • Fexofenadine at its recommended therapeutic dose of 120 mg is free from impairment effects on aspects of psychomotor function and hence can be used safely. (157)


  • In the present study, maternal exposure to loratadine does not appear to be associated with an increased risk of hypospodias when compared with other antihistamines, although it should be noted that the statistical precision of the risk estimates might be limited. (158)
  • Ketoconazole alters the pharmacokinetic profile of loratadine. Thus it should not be coadministered with loratadine. (159)
  • Loratadine reduces cough induced by ultrasonically nebulised distilled water (UNDW). The release of histamine may contribute to the chronic cough in patients with unexplained chronic cough or nasal disease. (160)
  • Loratadine plus pseudoephedrine improves nasal and asthma symptoms, pulmonary function and quality of life in patients with seasonal allergic rhinitis and concomitant mild asthma. (161)
  • Concomitant nefazodone treatment with loratadine is associated with marked QTc prolongation. (162)
  • Montelukast alone or in combination with loratadine is well tolerated and provides clinical and quality of life benefits for patients with seasonal allergic rhinitis. (163)
  • Levocetrizine is superior to loratadine for chronic idiopathic urticaria. (164)
  • The pharmacokinetics of loratadine in pediatric subjects is similar to that in healthy adult volunteers. The maximum concentration (Cmax) of loratadine and descarboethoxyloratadine were approximately 4 ng/ml each. The AUC of the metabolite was about 6 times that of loratadine. The elimination half half life of descarboethoxyloratadine averaged about 13.8 hr. (165)
  • Loratadine may be a promising option for severe, resistant pegfilgrastim induced bone pain. (166)
  • The onset of action following treatment with loratadine/ montelukast was 1 hour 15 min for total symptoms score as well as for nasal congestion. Loratadine/ montelukast was well tolerated. (167)


  • Rupatadine is a very good choice for seasonal allergic rhinitis due to its contribution to the improvement of nasal (including obstruction) and non-nasal symptoms to a similar degree as desloratadine. (168)
  • There is reduction in allergic rhinitis symptoms and improvement in nasal airflow in patients treated with desloratadine. (169)
  • There is no significant difference in efficacy whether desloratadine is given in the morning or in the evening. This gives the patients more flexibility in choosing dosing time. (170)
  • Desloratadine 5 mg once daily significantly decreased symptoms of chronic idiopathic urticaria and improved the quality of life. (171)
  • Desloratadine is effective for the relief of nasal and non nasal allergy symptoms. (172)
  • For persistent allergic rhinitis, the combination of montelukast and either desloratadine or levocetrizine is more effective than monotherapy with these agents. (173)
  • Desloratadine is a well tolerated and effective treatment of chronic idiopathic urticaria. (174)
  • Levocetrizine may be preferred to desloratadine as a treatment option for allergic rhinitis because of its faster onset of action and greater consistency of effect. (175)
  • There is a better overall protection of a single dose of levocetrizine compared to desloratadine in an nasal provocation test with grass pollen allergen. (176)
  • Pill esophagitis is a rare complication which occurs after taking desloratadine without liquid immediately before going to bed. (177)
  • Desloratadine syrup is safe and effective in the treatment of childhood atopic dermatitis. (178)
  • Desloratadine inhibits human skin mast cell activation and histamine release. (179)
  • Single dose co-administration of desloratadine and montelukast 2 h prior to allergen inhalation clinically abolished the late asthmatic response and eosinophil recruitment. (180)
  • Diphenhydramine 50 mg given for 1 week provides statistically significant and clinically superior improvements in symptoms compared with 5 mg of desloratadine in patients with moderate to severe seasonal allergic rhinitis. (181)
  • A single dose of desloratadine does not potentiate alchohol mediated CNS impairment. Desloratadine alone or in combination with alcohol is safe and well tolerated. (182)
  • Loaratadine and the active metabolites desloratadine and 3-OH-desloratadine are unlikely to affect the pharmacokinetics of coadministered drugs which are metabolized by these five cytochrome P-450 enzymes. (183)


  • Canine atopic dermatitis can be effectively treated with cetirizine. (184)
  • Cetirizine exerts its beneficial effects on viral myocarditis by suppressing expression of pro-inflammatory cytokines, genes related to cardiac remodelling in the herats of mice. (185)
  • Hypertonic saline aerosol can elicit airway obstruction in patients with moderate or severe chronic obstructive pulmonary disease. Cetirizine has some effects on hypertonic saline induced airway obstruction in patients with moderate to severe COPD. (186)
  • Cetirizine is well tolerated and effective in reducing symptoms of seasonal allergic rhinitis in patients undergoing controlled pollen challange. (187)
  • Cetirizine is approved by US FDA for allergic rhinitis in all age groups. It induces dystonic reactions in pediatric population. A case has v=been reported of involuntary movements associated with cetirizine use and discontinuation in adult. (188)
  • Cetrzine is considered to be safe in pregnancy. First trimester exposures to cetirizine is associated with no adverse pregnancy outcomes. (189)
  • In patients aged > 12 years who had allergic rhinitis, cetirizine us epromotes somnolence and decreased motivation to perform activities during the workday compared with loratadine. (190)
  • Recurrent acute hepatitis is associated with the use of cetirizine. (191)
  • Combined treatment with cetirizine and ranitidine in patients with functional dyspepsia shows a significant reduction in the severity and number of mast cells in gastric mucosa and leads to high rate of satisfaction among patients. (192)
  • Cetirizine is safe and effective in the treatment of allergic rhinitis. (193)
  • Cetirizine is proved to be more effective than terfenadine in controlling urticaria symptoms in patients with chronic idiopathic urticaria. (194)
  • Cetirizine may be useful antihistamine in the treatment of perennial allergic rhinitis for its long action, non-sedative property and convenient dosing schedule. (195)
  • Increasing the dose of cetirizine may lead to better control of chronic idiopathic urticaria. (196)


  • Levocetirizine is safe and effective treatment for allergic rhinitis, seasonal allergic rhinitis, perennial allergic rhinitis and chronic idiopathic urticaria. (197)
  • Levocetirizine does not produce ant deleterious effect on cognitive and psychometric functions in healthy male volunteers. (198)
  • Once daily levocetirizine is safe and effective in the treatment of allergic rhinitis and chronic idiopathic urticaria. (199)
  • Levocetirizine may be preferred to desloratadine as treatment option for allergic rhinitis because of its faster onset of action and greater consistency of effect. (200)
  • Levocetirizine has consistently high response rates, fast onset and a favorable side effect profile in patients with chronic idiopathic urticaria. (201)
  • Levocetirizine is superior to lotratadine in terms of safety and efficacy in patients with chronic idiopathic urticaria. (202) 
  • Levocetirizine improves the quality of life and symptoms and decrease the overall costs of the disease over the 6-month treatment period in patients with persistent allergic rhinitis. (203)
  • Levocetirizine 2.5 mg has comparable antihistaminic activity to cetrizine 5 mg, whereas its other enantiomer ucb 28557 has no pharmacodynamic effect suggesting that the antihistaminic properties of cetirizine observed in the management of allergic skin conditions are likely to be attributable to levocetrizine. (204)
  • The combined therapy with fluticasone furoate nasal spray and levocetirizine significantly suppressed the induced seasonal allergic rhinitis symptoms and delayed the onset of symptoms compared with levocetirizine monotherapy. (205)
  • Fexofenadine has the earliest onset of action while levocetirizine shows maximum inhibition of wheal response after three and six hours. (206)
  • Levocetirizine is a better option for treatment of seasonal allergic rhinitis both in terms of efficacy and safety when compared to cetirizine. (207)
  • Levocetirizine effectively reduces the activation and migration of antigen presenting cells to local draining lymph nodes and induces differentiation of Treg cells as one possible mechanism of its anti-inflammatory action. (208)
  • A double dose of levocetirizine leads to better control of histamine-induced flare, wheal response and itch in healthy donors. (209)
  • Second generation non-sedating antihistamines are recommended as first line therapy in the management of chronic spontaneous urticaria. If not responding, higher dose (up to four fold) of non sedating antihistamines is recommended. (210)


  • Compared to oral antihistamines, azelastine nasal spray has superior efficacy and more rapid onset of action in patients with seasonal allergic rhinitis. (211)
  • Azelastine nasal spray is effective in the treatment of vasomotor (perennial nonallergic) rhinitis. (212)
  • Azelastine nasal spray monotherapy is as effective as the combination of oral loratadine plus intranasal beclomethasone in treating moderate-to-severe symptoms of seasonal allergic rhinitis. (213)
  • A single oral dose of 4.4 mg of azelastine causes significant bronchodilation and attenuation of exercise-induced bronchoconstriction in patients with exercise induced asthma. (214)
  • A combination of azelastine and fluticasone propionate is highly effective in the treatment of moderate to severe seasonal allergic rhinitis. (215)
  • Azelastine posseses complementary antiallergic, antihistaminic, anti-inflammatory and antiasthmatic activities which may be of greater clinical benefit than an agent that interferes with a single mediator. (216)
  • Azelastine is more effective and yield higher patient satisfaction scores than olopatadine in the treatment of allergic cunjunctivitis. (217)
  • Azelastine, 6 mg twice per day can reduce the need for inhaled coticosteriods in patients with chronic bronchial asthma and not lead to a deterioration in pulmonary function. (218)
  • Azelastine is a genuine Ca++ antagonist that inhibits voltage gated Ca++ inward current and agonist-induced Ca++ release and Ca++ sensitization. (219)
  • The TNF-alpha secretion is suppressed by azelastine in a rat mast (RBL-2H3) cell line. This suggests that the release process of TNF-alpha in mast cells is regulated by a mechanism distinct from that of degranulation, and that in Ca2+-ionophore-stimulated cells, it is also different from that of transcription/production, and possibly involves protein kinase C activation. (220)
  • Azelastine, similar to capsaicin, exhibit direct activity on TRPV1 ion channels that may represent a novel mechanistic pathway explaining its clinical efficacy in nonallergic rhinitis. (221)
  • At the recommneded dosage (one spray per nostril twice daily), azelastine is a useful addition to the currently available therapies for allergic rhinitis in children. (222)
  • The inhibition of ovalbumin induced contraction of sensitized parenchymal tissues of Guinea pig in vitro study is dose dependent and controlled better with verapamil than azelastine. (223)
  • MP29-02 (a novel intranasal formulation of azelastine hydrochloride and fluticasone propionate in an advanced delivery system) is well tolerated and safe for long term use in the treatment of allergic rhinitis. (224)


  • MIzolastine is more active than loratadine on the wheal and lare inhibition from 3 up to 6 and 8 h respectively, as active as terfenadine on both parameters and as active as cetirizine on wheal inhibition while less active than cetirizine on flare inhibition at 2 and 12 h post-dosing. (225)
  • Cetirizine (10 mg) suppresses skin reactivity to histamine more effectively than mizolastine (10 mg) 24 h after intake in healthy volunteers. (226)
  • Mizolastine provides effective symptom relief in perennial allergic rhinitis together with a satisfactory safety profile. (227)
  • Mizolastine 10 mg once daily is at least as effective as cetirizine in relieving symptoms of seasonal allergic rhinoconjunctivitis, onset of action is rapid with clinical effects evident within 2 hours. (228)
  • Mizolastine is effective and well tolerated in the treatemnt of chronic idiopathic urticaria. (229)
  • Mizolastine is effective in the treatment of primary acquired cold urticaria. (230)
  • Mizolastine, 10 mg once daily at steady state is devoid of sedation and detrimental effect on skilled performance and memory. (231)
  • MIzolastine is an effective and well tolerated antihistamine in the treatemnt of seasonal allergic rhinitis, 10 mg is the optimal dose. (232)
  • MIzolastine has inhibitory effects on ultraviolet B-induced leukotriene B4 production and 5-lipoxygenase expression in normal human dermal fibroblasts in vitro. It may play a protective role in the pathogenesis of UV radiation-induced acute photodamage of the skin. (233)
  • Allergic reaction has been reported with mizolastine use. (234)
  • Mizolastine appears to be devoid of sedative effects in experimental models irrespective of the route of administration used. This predicts a lack of sedative action in humans with mizolastine at therapeutic doses. (235)
  • Mizolastine is effective and well tolerated in long term treatment of perennial allergic rhinoconjunctivitis. (236)
  • A single oral dose of mizolastine failed to induce subjective drowsiness and produces no detrimental effects on psychomotor performance or on short-term and long term memory in elderly patients. Thus mizolastine 10 mg can be safely used in elderly out patients as it preserves functions involved in activities of daily living. (237)


  • A superior efficacy of 20 mg of ebastine is compared with 10 mg ebastine and 10 mg cetirizine on the skin wheal response 24 h after the last dose of a 6 day long treatment.Ebastine has no negative effective on cognitive performance or mood. (238)
  • Ebastine is an effective and well tolerated antihistamine for the treatment of allergic rhinitis. (239)
  • Ebastine is an effective and generally well tolerated treatment for allergic rhinitis and chronic idiopathic urticaria. In addition to regular tablet formulation, it is available as a fast dissolving tablet, providing a treatment option that is particularly convenient for patients. (240)
  • Ebastine 20 mg once daily is significantly superior to loratadine 10 mg once daily at improving the rhinitis total symptom score throughout the day and at awakening over a 4 week period. Ebastine 20 mg and 10 mg doses are both efficacious and well tolerated in the treatment of seasonal allergic rhinitis. (241)
  • In nonatopic white subjects, inhibition of the response to histamine injection is significantly greater with ebastine 20 mg fast dissolving tablet compared with desloratadine 5 mg capsule and placebo after 1 and 5 days of administration. (242)
  • Ebastine at its recommended daily dose of 10 mg is free from disruptive effects on the CNS and should therefore prove valuable in the treatment of various allergic disorders in patients who wish to continue their activities without experiencing decrements in their psychomotor and cognitive abilities. (243)
  • Ebastine 20 mg have advantages over ebastine 10 mg and cetirizine 10 mg in terms of reduced time to achieve maximal efficacy and a superior level of efficacy in patients with more severe symptoms in patients with seasonal allergic rhinitis. (244)
  • Ebastine, an effective H1 rceptor antagonist with a prompt onset of action and a long duration of action, is suitable for once daily administration to children. (245)
  • Both CYP2J2 and CYP3A play important roles in ebastine sequential metabolism: dealkylation of ebastine and its metabolites is mainly catalyzed by CYP3A4, whereas the hydroxylation reactions are preferentially catalyzed by CYP2J2. (246)
  • Ebastine fast dissolving tablet is associated with a very high satisfaction rate and significant relief of rhinitis symptoms. (247)
  • Ebastine is an effective and well tolerated alternative to other non-sedating antihistamines in the treatment of chronic urticaria. (248)
  • Ebastine is efficacious 2nd generation antihistamine in treatment of allergic rhinitis in pediatric patients with minimal incidence of sedation. (249) 


  • Once daily rupatadine (10 and 20 mg) is an efficacious and safe treatment for the management of patients with perennial allergic rhinitis. (250)
  • The use of rupatadine is associated with heart rhythm disturbances. (251)
  • Rupatadine oral solution ( is effective in reducing nasal symptoms at 4 and 6 week and is well tolerated in the treatment of persistent allergic rhinitis in children. (252)
  • Rupatadine use is associated with Torsades de pointes. (253)
  • Rupatadine is superior to desloratadine in chronic idiopathic urticaria patients in terms of safety and efficacy because of its multiple mechanisms of action. (254)
  • Olopatadine is a better choice in seasonal allergic rhinitis in comparison to rupatadine due to its better efficacy and safety profile. (255)
  • Rupatadine is a dual inhibtor of histamine H1 and well tolerated treatment for allergic rhinitis and chronic urticaria. It possesses a broader profile of anti-inflammatory properties inhibiting both inflammatory cells and a range of mediators involved in the early and late phase inflammatory response. (256)
  • Rupatadine 20 mg/d shows high efficacy and is well tolerated in the treatment of acquired cold urticaria. (257)
  • Platelet activating factor (PAF) stimulates human mast cell release of proinflammatory mediators that is inhibited by rupatadine. This action endows rupatadine with additional properties in treating allergic inflammation. (258)
  • Rupatadine promotes the resolution of pulmonary inflammation and fibrosis by attenuating the PAF mediated senescence response. Rupatadine holds promise as a novel drug to treat the devastating disease of pulmonary fibrosis. (259)
  • Concomitant intake of food with a single 20 mg oral dose of rupatadien exhibits a significant increase in  rupatadine bioavailability. Despite the absene of bioequivalence, the drug is well tolerated under fed and fasting conditions, an dno major changes in severity and/ or prevalence of adverse events were reported. (260)
  • Rupatadine 10 mg may be valuable and safe alternative for symptomatic treatment of seasonal allergic rhinitis. (261)


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