SEARCH · PubMed Health

Results for “Administration, Intranasal”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources

PubMed1986

Protection of mice from lethal influenza: evidence that defective interfering virus modulates the immune response and not virus multiplication.

Intranasal administration of defective interfering (DI) influenza virus (A/WSN) ensured the survival of 80% of C3H mice otherwise lethally infected with WSN by the intranasal route, whereas a control group which received beta-propiolactone-inactivated DI virus in place of DI virus died at 7.4 days post-infection. DI virus-treated mice developed significantly less lung consolidation than controls although qualitatively the cellular pathology in the two groups was indistinguishable. Surprisingly, in view of the accepted mode of action of DI virus interference, multiplication of infectious virus in the lung, production of viral haemagglutinin (HA) antigen and neuraminidase, and the distribution and amount of viral antigen in cells as shown by immune labelling were unaffected by the presence of active DI virus. Furthermore, assays of lung extracts showed that DI virus was not stimulating significantly greater amounts of interferon than the control inactivated DI virus. An alternative explanation arises from the fact that the pathology of influenza in inbred mice is immune (T lymphocyte)-mediated. Thus, since there is no evidence that DI virus affects virus multiplication we suggest that DI virus is responsible for ameliorating the damaging host responses. Another aspect of the immune response modulated by DI virus was the enhancement of local haemagglutination-inhibiting (HI) antibody in the lung, with peak increases of up to 10-fold over the relevant controls being demonstrated at 5 days after infection. This antibody was presumably complexed to HA antigen in the lung as activity was only demonstrated after elution at low pH. It had no detectable neutralizing activity (less than 10% HI: neutralization ratio of convalescent serum) which accounts for the coexistence of local antibody and virus infectivity. Mice infected with virus alone or which received beta-propiolactone-inactivated DI virus in addition to a lethal dose of WSN did not develop significant amounts of lung antibody. No differences were seen in serum HI titres. The increased level of antibody could not be attributed to the presence of greater amounts of HA antigen in lungs of mice treated with DI virus, as ELISA showed no significant difference from control preparations. The possibility that the two modulated immune responses are linked through HI antibody blocking access of T cells to cell membrane-borne HA antigen is discussed.

Animals↗

PubMed2000

Role of pulmonary alveolar macrophages in defense of the lung against Pseudomonas aeruginosa.

Alveolar macrophages (AM) provide one of the first lines of defense against microbial invasion in the lower airways. The role of AM in the clearance of Pseudomonas aeruginosa in mice after intrapulmonary challenge was evaluated. AM were depleted by intranasal administration of liposome-encapsulated dichloromethylene diphosphonate. At 24 h following the instillation of liposomes, a sublethal dose of P. aeruginosa was inoculated intranasally. Spleen, liver, and lung tissue was then evaluated for viable bacteria and for histopathology. AM depletion of 78 to 88% did not affect the survival rate of infected mice or clearance of P. aeruginosa from the spleen, liver, or lung, compared to the control group, but the mice's susceptibility to Klebsiella pneumoniae was greatly enhanced. The recruitment of neutrophils to the lung was also not affected. Freshly explanted AM were not competent to phagocytose unopsonized P. aeruginosa but were able to phagocytose zymosan particles. Further studies were conducted to assess the in situ phagocytic activities of AM. Three hours after the intranasal instillation of P. aeruginosa or other particles, bronchoalveolar lavage was performed. AM phagocytosis of zymosan particles and latex beads exceeded that of P. aeruginosa. Neutrophils were recruited to the lung in response to a high-dose bacterial challenge. These results suggest that AM do not play an important role in defense of the lung against P. aeruginosa.

Animals↗

PubMed2002

Escherichia coli heat-labile enterotoxin B subunit prevents autoimmune arthritis through induction of regulatory CD4+ T cells.

OBJECTIVE: The receptor-binding B subunit of Escherichia coli heat-labile enterotoxin (EtxB) is a highly stable, nontoxic protein that is capable of modulating immune responses. This study was conducted to determine whether mucosal administration of EtxB can block collagen-induced arthritis (CIA) and to investigate the mechanisms involved. METHODS: Clinical arthritis in DBA/1 mice was monitored following mucosal administration of EtxB on 4 occasions. The dependence of disease prevention on receptor binding by EtxB and the associated alterations to the immune response to type II collagen (CII) were assessed. Adoptive transfer experiments and lymph node cell cocultures were used to investigate the underlying mechanisms. RESULTS: Both intranasal and intragastric delivery of EtxB were effective in preventing CIA; a 1-microg dose of EtxB was protective after intranasal administration. A non-receptor-binding mutant of EtxB failed to prevent disease. Intranasal EtxB lowered both the incidence and severity of arthritis when given either at the time of disease induction or 25 days later. EtxB markedly reduced levels of anti-CII IgG2a antibodies and interferon-gamma (IFNgamma) production while not affecting levels of IgG1, interleukin-4 (IL-4), or IL-10. Disease protection could be transferred by CD4+ T cells from treated mice, an effect that was abrogated upon depletion of the CD25+ population. In addition, CD4+CD25+ T cells from treated mice were able to suppress anti-CII IFNgamma production by CII-primed lymph node cells. CONCLUSION: Mucosal administration of EtxB can be used to prevent or treat CIA. Modulation of the anti-CII immune response by EtxB is associated with a reduction in Th1 cell reactivity without a concomitant shift toward Th2. Instead, EtxB mediates its effects through enhancing the activity of a population of CD4+ regulatory T cells.

Adjuvants, Immunologic↗

PubMed1989

Molecular mechanism of complex infection by bacteria and virus analyzed by a model using serratial protease and influenza virus in mice.

We examined the effect of a serratial exoprotease on the pathogenesis of influenza virus infection in mice as a model of complicated respiratory infection by bacteria and virus in humans. The 56-kilodalton (56-kDa) protease from Serratia marcescens was administrated intranasally to mice at a dose of 10, 20, or 40 micrograms from day 0 to day 3 after inoculation of the influenza virus. Administration of the protease resulted in remarkable enhancement of the lethal effect of the virus and enhancement of pathological changes in the lungs. Influenza virus replication, determined by plaque-forming assay, was accelerated by the protease. Namely, we found a 100-fold increase in virus yield by day 2. The 56-kDa protease caused generation of plasmin activity in the lungs. In vitro experiments showed that plasmin greatly enhanced the yield of influenza virus, although the effect of the 56-kDa protease by itself was much lower than that of plasmin. Furthermore, the 56-kDa protease could induce plasmin production indirectly via activation of plasminogen by the Hageman factor-dependent cascade in the in vitro system. We conclude that this major serratial exoprotease has a deleterious effect on mice infected with influenza virus and that this effect seems to result from enhancement of viral growth by indirect acceleration of plasmin generation induced by the protease.

Animals↗

PubMed2002

Pharmacokinetics of ketotifen fumarate after intravenous, intranasal, oral and rectal administration in rabbits.

The pharmacokinetics of ketotifen fumarate (KF) was examined after administration in rabbits through four different routes (intravenous, intranasal, oral and rectal). The time-course of the plasma concentration of KF after intravenous administration (1 mg/kg dose) fitted a two-compartment open model. KF was rapidly absorbed and showed a high plasma concentration within 0.33 h after intranasal administration. The absolute bioavailability of KF after intranasal administration was 66%. After oral administration at a dose of 1 mg/kg, the plasma concentration of KF was below the detection limit of HPLC analysis. Even at 5 mg/kg, the value of the area under the plasma concentration-time curve (AUC) after oral administration of KF was significantly lower than that after intranasal administration of 1 mg/kg. Oral bioavailability was only 8%. The very low bioavailability of KF after oral administration might be due to the first-pass effect in the liver. We also prepared suppositories containing KF (1 mg/kg) for rectal administration in rabbits. After rectal administration, KF was rapidly absorbed and its bioavailability was 34%. These results indicated that the intranasal route appears the most effective for administering KF, and that rectal administration may be superior to oral administration in terms of bioavailability.

Administration, Intranasal↗

PubMed2002

Mucosal tolerance to a bacterial superantigen indicates a novel pathway to prevent toxic shock.

Enterotoxins with superantigenic properties secreted during systemic Staphylococcus aureus infection are responsible for toxic shock. We show that intranasal administration of staphylococcal enterotoxin A (SEA), but not a recombinant SEA lacking superantigenic activity, protected mice against lethal systemic SEA challenge. Protection was superantigen specific since intranasal exposure to SEA would not protect against death caused by subsequent toxic shock syndrome toxin 1 systemic challenge. Protection was neither due to selective depletion of SEA-specific T-cell receptor Vbeta families nor due to production of neutralizing anti-SEA antibodies. Importantly, the production of interleukin 10 (IL-10) induced by "tolerization" (that is, by the induction of immunological tolerance) contributed to the observed protection against lethal superantigen-triggered disease. In support of this notion we found that (i) significantly increased levels of IL-10 in sera of "tolerized" animals (that is, animals rendered tolerant) and (ii) IL-10(-/-) mice could not be tolerized by mucosal SEA administration. Altogether, this is the first study to show that mucosal tolerance to a superantigen is readily triggered by means of immunodeviation.

Animals↗

PubMed2000

The route of administration of an immunodominant peptide derived from heat-shock protein 65 dramatically affects disease outcome in pristane-induced arthritis.

Previous studies have shown that immunization of mice with an immunodominant epitope from heat-shock protein 65 (hsp 65) (amino acids 261-271) can protect from the development of pristane-induced arthritis (PIA) and this protection is mediated by an antigen-specific T helper type 2 (Th2) cytokine response. Here we confirm these findings and show that frequent intranasal administration of this peptide exacerbates disease. In naive mice given peptide intranasally an antigen-specific T-cell population is systemically activated similar to that induced by peptide immunization in incomplete Freund's adjuvant. Thus, a paradox exists whereby apparently similar peptide-specific populations are either associated with protection from, or exacerbation of, PIA. However, comparison of cytokine profiles reveals differences between these two cell populations. Peptide inhalation induces the production of Th1-type cytokines (interferon-gamma) whereas intraperitoneal immunization leads to the production of Th2-type cytokines (interleukin-4, interleukin-5 and interleukin-10) by splenic T cells upon stimulation with peptide. Thus, for the application of nasal 'tolerance' in clinical medicine, it is important to identify antigens and dosing regimes that counteract but do not activate adverse immune responses.

Animals↗

PubMed2000

Infection of intestinal epithelial cells and development of systemic disease following gastric instillation of murine gammaherpesvirus-68.

Murine gammaherpesvirus-68 (gammaHV-68) induces a lymphocytosis in mice and establishes a latent infection of B lymphocytes following intranasal administration in anaesthetized animals. Because gammaHV-68 is a gammaherpesvirus, it has been used as a model to understand the pathogenesis of Epstein-Barr virus (EBV) and human herpesvirus-8 (HHV-8) infections. In this study, we investigated the unlikely possibility that gammaHV-68 could survive the harsh gastrointestinal environment to efficiently infect intestinal epithelial cells, and then disseminate from mucosal sites to cause systemic disease. Surprisingly, oral administration, or gastric instillation which by-passed the oral cavity, readily caused a systemic lymphocytosis and established a latent infection in splenic leukocytes. The finding that gammaHV-68 could readily infect adult mice following gastric instillation strongly suggested that intestinal epithelial cells could be productively infected. Unlike the more routinely used method of intranasal inoculation, gammaHV-68 given intragastrically resulted in lytic virus, viral RNA and viral DNA being present in isolated intestinal epithelial cells. Furthermore, gammaHV-68 RNA and DNA, but not latent virus, could be detected in epithelial cells as long as 30 days post-infection, suggesting that some of these cells might be persistently infected. Taken together, these studies demonstrate that gammaHV-68 can survive passage through the gastrointestinal tract and infect intestinal epithelial cells. Following infection of gut epithelial cells, gammaHV-68 can disseminate from mucosal sites to induce a systemic lymphocytosis which is similar to the disease induced following intranasal inoculation.

Administration, Oral↗

PubMed1989

Experimental transmission and electron microscopic demonstration of the virus of haemorrhagic disease of rabbits in Czechoslovakia.

Intramuscular administration of the filtrate of organ suspensions, prepared from a dead rabbit, killed 62.9% of inoculated rabbits within 1 to 5 days, while 93.3% died after intranasal administration of the same inoculum. The virus survived freeze-drying and was resistant to treatment with 0.4% formaldehyde when incubated at 37 degrees C for 1 hour and 4 degrees C for the subsequent 12 hours, but lost its infectivity when the treatment was prolonged to 3 hours at 37 degrees C and 3 days at room temperature. Its infectivity was also inhibited by reconvalescent serum. The virus could not be detected after 3 passages in primary rabbit kidney cell cultures. Electron microscopy of negatively stained preparations demonstrated icosahedral virus particles with a diameter of 29 to 33 nm without an envelope. Accurate morphological classification has not yet been completed. Incubation with a reconvalescent serum, diluted 1:20 or 1:40, resulted in the formation of immune complexes, detectable by electron microscopy.

Animals↗

PubMedDate not supplied

[The sensitizing properties of the ballast admixtures in human leukocyte interferon].

Due to the features of its production technology, human leukocyte interferon (HLI) for intranasal administration is likely to contain ovalbumin (OA). Commercial batches of HLI were tested for the presence of OA responsible for the sensitizing effect of HLI given intranasally. The content of OA in commercial batches of HLI was shown to vary widely and to exceed by far the concentrations having the sensitizing effect. As a result of these studies, the upper limit of OA content was established and the technology of HLI production was modified. These measures permitted production of commercial batches of HLI with OA content not exceeding 0.05 micrograms/ml.

Anaphylaxis↗

PubMed1978

Reduction of respiratory tract binding of benzo[a]pyrene in mice by immunization.

Male inbred A/J mice immunized by combined ip and intranasal administration of a bovine serum albumin conjugate of 5-fluoro-12-methylbenzanthryl-7-acetic acid developed tracheal antibodies capable of binding the carcinogen benzo[a]pyrene (BP). Immunized mice administered 92 ng of [3H]BP intranasally exhibited a one-third reduction in BP content in respiratory tract tissues (nose and trachea) when compared with control mice 20 hours after BP administration.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2001

Six month administration of gelified intranasal insulin in 16 type 1 diabetic patients under multiple injections: efficacy vs subcutaneous injections and local tolerance.

OBJECTIVE: Nasal insulin administration is a potential route for intensive insulin management, less invasive and more rapid than subcutaneous injections. Previous studies have shown poor bioavailability (less than 15%) with nasal insulin administration with various absorption enhancers. The aim of the study was to evaluate in type 1 diabetic patients, the metabolic efficacy and local tolerance of a new gelified sprayed nasal insulin containing glychocolate and methylcellulose as absorption promoters. MATERIAL AND METHODS: The study was conducted in 16 type 1 diabetic patients (HbA1c 8.6+/-0.2%) in a cross-over trial including 2 six month randomized periods: a) NPH twice daily + 3 pre-prandial nasal insulin doses + nasal supplementation in case of unexpected hyperglycaemia; b) NPH twice daily + 3 pre-prandial regular insulin injections. End points were HbA1c levels, hypoglycaemic episodes and tolerance evaluated at month 0, 2, 6 and 8 on clinical symptoms and objective nasal assessments. RESULTS: Four patients were withdrawn because of nasal burning (3 cases) and persistent sinusitis (1 case), and one patient had purulent sinusitis at the month 6 examination. At month 6, HbA1c levels were comparable (8.3 +/- 0.1 vs 8.6 +/- 0.1%, m +/- SEM, NS) for nasal and subcutaneous period respectively. The number of hypoglycaemic events was identical during the 2 periods (88 episodes). Nasal tolerance with the gelified form was better than with the already reported lyophilized form but, when present, symptoms were more marked, suggesting a potentiating additional role of methylcellulose excipient on nasal intolerance. CONCLUSIONS: 1) Gelified nasal insulin is as efficient as subcutaneous regular insulin in type 1 diabetic patients. 2) Other galenic forms should be investigated to improve nasal tolerance and bioavailability.

Administration, Intranasal↗

PubMed1998

IgA antibody-forming cell responses in the nasal-associated lymphoid tissue of mice vaccinated by intranasal, intravenous and/or subcutaneous administration.

Effects of a single intranasal (i.n.), subcutaneous (s.c.) or intravenous (i.v.) vaccination and their combined vaccination of priming and boosting on a primary and a secondary IgA antibody forming cell (AFC) response were examined in the nasal associated lymphoid tissue (NALT), spleen and popliteal lymph nodes (pLNs) of BALB/c mice. Mice were primed with the vaccine prepared from A/Yamagata/120/86 (H1N1) together with a cholera toxin-adjuvant and boosted with the same vaccine 3 weeks later. Three days after boosting, IgA-AFC responses in each lymphoid tissue were measured as an index of the immunological memory that mediates a secondary IgA-AFC response. Single i.n. vaccination induced a greater primary IgA-AFC response in the NALT not only than that in the spleen or pLNs, but also than that induced by single i.v. or s.c. vaccination. The combination of i.n. priming and i.n. boosting afforded a greater anamnestic IgA-AFC response in the NALT not only than that in the spleen or pLNs, but also than that induced by any other combinations of priming and boosting (i.n.-i.v., i.n.-s.c., s.c.-i.n., s.c.-i.v., and s.c.-s.c.). These results showed that i.n. priming induced a greater primary IgA-AFC response in the NALT and simultaneously induced the immunological memory that mediated a greater secondary-type AFC response following i.n. boosting in the NALT.

Administration, Intranasal↗

PubMed2007

The effect of MK-0524, a prostaglandin D(2) receptor antagonist, on prostaglandin D (2)-induced nasal airway obstruction in healthy volunteers.

INTRODUCTION: Nasal congestion in allergic rhinitis results from tissue edema and vasodilatation in the nasal mucosa. Of the mediators released by mast cells in response to allergens, prostaglandin (PG) D(2) is regarded as the most potent inducer of nasal congestion. Intranasal administration of PGD(2) reproduces the nasal blockade experienced by patients with seasonal allergic rhinitis (SAR) via its action on the PGD(2) (DP) receptor to induce nasal vasodilatation. Intranasal challenge with PGD(2) can be a useful tool for evaluating DP-receptor antagonists. OBJECTIVE: The main purpose of this study was to examine the ability of MK-0524, a DP receptor antagonist in development for the treatment of SAR, to block PGD(2) induced nasal congestion in healthy volunteers. METHODS: To this end, a double-blind, placebo-controlled, randomized, 3-period study was performed in 15 healthy subjects. During each period, subjects received MK-0524 25 mg, MK-0524 100 mg or placebo qd for 3 days. Twenty-four hours following the last dose, nasal provocations with PGD(2) were performed to determine the PD(75), which is the intranasal dose of PGD(2) that provokes a 75% increase in baseline total nasal airway resistance as performed by active anterior rhinomanometry. RESULTS: Following treatment with MK-0524, the PD(75) (mean+/-SD) was significantly shifted from 15.8 +/- 18.3 mug/nostril during the placebo period to more than 512 mug/nostril both following the 25- and 100-mg (maximum challenge dose tested) dose regimen. CONCLUSION: Whether this >45 fold increase in PD(75) will induce a clinically meaningful effect of MK-0524 will require clinical study in participants with SAR.

Administration, Oral↗

PubMed1993

Pre-ovulatory progesterone growth rate in patients treated with gonadotrophin-releasing hormone agonist and outcome of in-vitro fertilization.

The present study was undertaken to assess whether the increase in serum progesterone concentration following the administration of human chorionic gonadotrophin (HCG) may have predictive value on the in-vitro fertilization (IVF) success rate. Progesterone concentration on the day of HCG administration and the increase in progesterone concentration on the following day were evaluated in 140 consecutive patients undergoing IVF with embryo transfer. Stimulation protocol in all study patients entailed intranasal administration of short-acting gonadotrophin-releasing hormone agonist (GnRHa) buserelin and human menopausal gonadotrophin. A pregnancy rate of 37.2% was achieved when at least three embryos were transferred. The only significant difference between conception and non-conception cycles was found in serum progesterone concentrations after HCG administration (P < 0.01), whereas the mean progesterone concentration on the day of HCG did not differ. No difference in other hormonal or cycle parameters was observed. The increase in progesterone concentration was significantly greater in the group of patients who achieved pregnancy than in the group who did not (2.2 +/- 0.2 versus 1.6 +/- 0.1 ng/ml, respectively; P < 0.01). A critical breakpoint in serum progesterone was arbitrarily determined at 1 ng/ml. An increase in progesterone concentration > or = 1 ng/ml when three or more embryos were transferred was associated with a positive predictive value for pregnancy of 40.4% (sensitivity of 94.7%), whereas a negative predictive value of 86.7% was obtained when this value was < 1 ng/ml. These findings indicate that an adequate rise in serum progesterone following HCG administration provides useful information about the possible outcome of the treated cycle.

Adult↗

PubMed1986

Central diabetes insipidus in children. V. Oral treatment with a vasopressin hormone analogue (DDAVP).

1-deamino-8-D-arginine-vasopressin, or DDAVP, a potent long acting antidiuretic analogue of AVP, is the treatment of choice in central diabetes insipidus (DI). We have studied the clinical and biological effect in 10 children with DI treated with peroral administration of DDAVP. During a dose ranging study in hospital, followed by 6 months of treatment at home, this peroral DDAVP tablet proved to be as effective as the intranasal administration of DDAVP and was preferred by the patients. Even doses as small as 12.5 micrograms, have an effect on diuresis and urinary osmolality. Therapeutic effects start at above 100 micrograms. During the dose ranging study 200 micrograms peroral DDAVP produced antidiuresis varying from 8 to 12.5 hours, in different patients. The recommended dose is 100-300 micrograms 2-3 times a day. This treatment offers an important alternative to that traditionally used and constitutes one of the first examples of a peptide conserving its biological activity after gastrointestinal transport.

Administration, Oral↗

PubMed1966

Isolation of a Soluble Resistance-Enhancing Factor from Mycobacterium phlei.

Fox, Alfred E. (Warner-Lambert Research Institute, Morris Plains, N.J.), Joachim Anschel, George L. Evans, Raam R. Mohan, and Benjamin S. Schwartz. Isolation of a soluble resistance-enhancing factor from Mycobacterium phlei. J. Bacteriol. 92:285-290. 1966.-Extraction of a crude cell wall preparation from Mycobacterium phlei with 20% urea yielded a fraction which induced a state of enhanced resistance to microbial challenge. The resulting soluble extract, after removal of the urea, represented a 15% yield of solids with the separation of the biologically active component(s) and elimination of toxicity. Single oral or subcutaneous submicrogram doses of this material induced a prolonged state of increased resistance to subsequent challenge with Salmonella enteritidis in mice. This effect appeared as early as 2 hr after oral administration and persisted for at least 30 days. Protection against experimental infection with Staphylococcus aureus was also demonstrated. Resistance to viral challenge with influenza type A was observed after intranasal administration of the M. phlei extract to mice. The isolated material was found to contain carbohydrate, protein, nucleic acids, and lipids. The lipids represented 60% of the total solids, and were all short-chain fatty acids. No toxic effects, including pyrogenicity, could be demonstrated after oral or parenteral administration of this preparation.

Journal Article↗

PubMed1998

ARL 15849: a selective CCK-A agonist with anorectic activity in the rat and dog.

Cholecystokinin octapeptide (CCK-8) and the peptide analog ARL 14294, formerly FPL 14294, [Hpa(SO3H)-Met-Gly-Trp-Met-Asp-N(Me)Phe-NH2], have been reported to induce satiety by interaction with the CCK-A receptor subtype. ARL 15849 [Hpa(SO3H)-Nle-Gly-Trp-Nle-N(Me)-Asp-Phe-NH2] is an improved ARL 14294 analog with enhanced CCK-A receptor selectivity, greater stability, and a longer duration of action. The affinity of ARL 15849 for the CCK-A receptor (Ki = 0.034 nM) is 6,600 fold greater than for the CCK-B receptor (Ki = 224 nM), whereas CCK-8 and ARL 14294 are nonselective. Although comparable in potency to contract isolated gallbladder and induce pancreatic phosphatidylinositol hydrolysis, ARL 15849 is 3- and 100-fold more potent than ARL 14294 and CCK-8, respectively, to inhibit 3-h feeding in rats. The duration of feeding inhibition was significantly longer for ARL 15849 (>5 h), compared to equipotent doses of ARL 14294 (3 h), and CCK-8 (1 h). Intranasal administration of ARL 15849 inhibits feeding in beagle dogs with a greater separation between doses that induce emesis and those that inhibit feeding. Therefore, ARL 15849 is a potent, selective, intranasally active anorectic agent which may be useful in the treatment of eating disorders.

Animals↗