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PubMed1985

Anticonvulsant action in the epileptic gerbil of novel inhibitors of GABA uptake.

Two novel inhibitors of GABA uptake, namely SKF 89976-A (N-[4,4-diphenyl-3-butenyl]-nipecotic acid) and SKF 100330-A (N-[4,4-diphenyl-3-butenyl]-guvacine) were tested for anticonvulsant effects in genetically seizure-prone gerbils. Both compounds proved able to block major (generalized tonic-clonic) seizures initiated in gerbils by air blast stimulation. The respective anticonvulsant ED50s for SKF 100330-A and SKF 89976-A were 1.6 and 4.1 mg/kg i.p., respectively. Comparison with other GABA uptake inhibitors, namely ethyl and methyl esters of (-)- and (+)-nipecotic acid and (+/-)-cis-4-hydroxynipecotic acid, showed that the novel uptake inhibitors were considerably more potent. Similarly, comparison with common antiepileptic drugs demonstrated that SKF 100330-A and SKF 89976-A were more potent than phenobarbital and valproic acid to block seizures in gerbils. Only benzodiazepines surpassed these GABA uptake inhibitors in anticonvulsant potency. Observation of behaviour indicated that the novel compounds exerted no side-effects in anticonvulsant doses. These data indicate that SKF 100330-A and SKF 89976-A deserve interest as potential antiepileptic drugs with a very selective mechanism of action.

Animals↗
PubMed1976

The in vivo inactivation of GABA and other inhibitory amino acids in the cat nervous system.

In cats anaesthetised with pentobarbitone, the effect of inhibitors of the in vitro cellular uptake of GABA were tested on the responses of single central neurones to GABA and other depressant amino acids. (4)- AND (-)-nepecotic acid, (4)-2,4-diaminobutyric acid (DABA) and 2,2-dimethyl-beta-alanine, enhanced the action of GABA on spinal, cerebellar and cerebral cortical neurones. In the spinal cord DABA, and to a less estent (-)-nipecotic acid, enhanced the action of beta-alanine, whereas the actions of glycine and taurine were unaffected by DABA and reduced by (-)-nipecotic acid. In the cerebellum and cerebral cortex, these two substances enhanced the action of GABA, usually to a greater extent than that of beta-alanine and taurine, although this specificity was not marked. The GABA-mediated basket cell inhibition of Purkinje cells in the cerebellum was unaffected by DABA and (-)-nipecotic acid, and neither substance appears suitable for determining the role of uptake processes in the inactivation of synapitcally released GABA. Quantitatively these in vivo results agree more closely with recent vitro uptake studies in cat tissue than the previously published data on rat cerebral cortex and dorsal root ganglia, and the observations provide further evidence for the importance of cellular uptake in maintaining low extraneuronal concentrations of inhibitory amino acid transmitters.

Action Potentials↗
PubMed1984

Gabaergic modulation of mouse-killing in the rat.

When GABA-potentiating compounds were administered IP to rats with prior experience of mouse-killing behaviour, a reduction of killing was observed with gamma-vinyl GABA (200 and 400 mg/kg) and nipecotic acid amide (400 mg/kg), while no significant effect was noted following injection of dipropylacetate or THIP. The inhibitory effects of gamma-vinyl GABA and nipecotic acid amide were not reversed by subsequent injection of picrotoxin and were associated with sedation as observed in open field and actograph tests. When GABA-potentiating compounds were administered to food-deprived rats exposed for the first time to a mouse (initial elicitation), administration of gamma-vinyl GABA, dipropylacetate, nipecotic acid amide or THIP increased the incidence of mouse-killing behaviour. Conversely, the incidence of mouse-killing under the same conditions was reduced following injections of picrotoxin. These results do not support the hypothesis that the general activation of GABAergic mechanisms inhibits mouse-killing behaviour in rats. On the contrary, data obtained in naive animals suggest that potentiation of these mechanisms actually facilitates the initial elicitation of this behaviour.

Aggression↗
PubMed1997

In vivo characterization of extracellular GABA release in the caudate nucleus and prefrontal cortex of the rhesus monkey.

Extracellular gamma amino butyric acid (GABA) levels were measured in the caudate nucleus and the prefrontal cortex of the rhesus monkey brain using in vivo microdialysis under isofluorane gas anesthesia. Evoked GABA release was investigated for voltage sensitivity and calcium (Ca2+) dependency. There was a multifold increase in extracellular GABA levels following local perfusion with: (1) high potassium (50 mM, KCI), (2) veratridine (10 microM), and (3) the GABA releasing agent and uptake blocker, (-) nipecotic acid (1 mM). Release of GABA was significantly reduced when veratridine or (-) nipecotic acid were coinfused in Ca(2+)-free cerebrospinal fluid (CSF). Coinfusion of nipecotic acid with TTX (10 microM) also resulted in attenuation of evoked GABA release. These results suggest that GABA levels recovered using in vivo microdialysis, from the caudate nucleus and the prefrontal cortex in the rhesus monkey, derive in significant part from vesicular pools and the exocytotic process is both Ca(2+)-dependent and voltage-sensitive.

Animals↗
PubMed2001

Efflux of a suppressive neurotransmitter, GABA, across the blood-brain barrier.

In this study, GABA efflux transport from brain to blood was estimated by using the brain efflux index (BEI) method. [3H]GABA microinjected into parietal cortex area 2 (Par2) of the rat brain was eliminated from the brain with an apparent elimination half-life of 16.9 min. The blood-brain barrier (BBB) efflux clearance of [3H]GABA was at least 0.153 mL/min/g brain, which was calculated from the elimination rate constant (7.14 x 10(-2) x min(-1)) and the distribution volume in the brain (2.14 mL/g brain). Direct comparison of the apparent BBB influx clearance [3H]GABA (9.29 microL/min/g brain) and the apparent efflux clearance (153 microL/min/g brain) indicated that the efflux clearance was at least 16-fold greater than the influx clearance. In order to reduce the effect of metabolism in the neuronal cells following intracerebral microinjection, we determined the apparent efflux of [3H]GABA in the presence of nipecotic acid, a GABA transport inhibitor in parenchymal cells, using the BEI method. Under such conditions, the elimination of [3H]GABA across the BBB showed saturation and inhibition by probenecid in the presence of nipecotic acid. Furthermore, the uptake of [3H]GABA by MBEC4 cells was inhibited by GABA, taurine, beta-alanine and nipecotic acid in a concentration-dependent manner. It is likely that GABA inhibits the first step in the abluminal membrane uptake by brain endothelial cells, and that probenecid selectively inhibits the luminal membrane efflux transport process from the brain capillary endothelial cells based on the in vivo and in vitro evidence. The BBB acts as the efflux pump for GABA to reduce the brain interstitial fluid concentration.

Animals↗
PubMed1984

Inhibition of GABA uptake potentiates the conductance increase produced by GABA-mimetic compounds on single neurones in isolated olfactory cortex slices of the guinea-pig.

Membrane potential and input conductance were recorded in single neurones in slices of guinea-pig olfactory cortex in vitro. gamma-Aminobutyric acid (GABA) and GABA-mimetic compounds were applied by bath-perfusion. Potency was measured as the concentration required to double the input conductance. The potency of GABA was increased (i.e. the equi-effective concentrations were reduced) by 15.5 +/- 2.3 times (mean +/- s.e. mean) on reducing external [Na+] from 144 to 20 mmol l-1, by replacement with Mg2+. Corresponding potency changes for other agonists were + 10.8 +/- 2.5 for 3-aminopropanesulphonic acid (3-APS); 3.25 +/- 1.06 for isoguvacine and 2.43 +/- 0.69 for muscimol. Nipecotic acid (0.5 mM) produced the following increases in potency: GABA 2.68 +/- 0.02; 3-aminopropanesulphonic acid, 3.11 +/- 0.07; isoguvacine, 1.92 +/- 0.34; muscimol, 2.24 +/- 0.17. The concentration of GABA in the bathing fluid necessary to double input conductance increased with increasing depth of the recording site from the cut surface. The apparent potency fell 10 times for each 60 micron depth increment up to 150 micron. The recording depth also affected the apparent potency of muscimol and 3-APS but to a lesser extent. Reduction of external [Na+] reduced the depth-dependence of both GABA and 3-APS potency. No clear change in the duration of the recurrent inhibitory postsynaptic conductance could be detected in the presence of 0.5 mmol l-1 nipecotic acid. 6 It is suggested that agonist uptake by a Na+-dependent, nipecotic acid-sensitive mechanism severely attenuates the responses of olfactory neurones to exogenous GABA and to its analogues 3-APS, muscimol and isoguvacine, but has little immediate influence on the duration of the GABA-mediated inhibitory postsynaptic conductance.

Animals↗
PubMed1983

Synaptic interactions in the GABA system during postnatal development in retina.

Using biochemical analyses, we have demonstrated the presence of a high-affinity, sodium- and temperature-dependent uptake system for GABA in the retinas of newborn rabbits. The activity of this system two days after birth is approximately 70 percent of adult values, slowly increasing to adult level by postnatal day 6-8. An intraocular injection nipecotic acid (final concentration = 10 mM) into one-day-old rabbit pups resulted in a 60 percent inhibition in uptake activity. In order to study the possible role of the GABA uptake system in retinal development, we have determined the consequences of blocking GABA uptake with nipecotic acid on the postnatal development of post-synaptic GABA receptors, as measured by 3H-muscimol binding. Nipecotic acid treatment caused a significant increase in receptor binding in retinas prior to eye opening, with the maximal stimulation being one day after the intraocular injection. Our data indicate that the development of GABA receptor sites is influenced by the activity of the GABA uptake system and suggest that GABA may function as a trophic factor in the developing rabbit retina.

Animals↗
PubMed1996

Effects of GABA uptake inhibitors on posthypoxic myoclonus in rats.

Male Sprague-Dawley rats developed posthypoxic myoclonus following 10-min cardiac arrest and resuscitation. Previous results showed that dysfunction of central GABAergic neurotransmission may contribute to the disease. In current studies, effects of GABA uptake inhibitors, guvacine hydrochloride (1,2,5,6-tetrahydro-3-pyridine carboxylic acid hydrochloride) and (+/-)-cis-4-hydroxynipecotic acid ([+/-]-cis-4-hydroxy-3-piperidine carboxylic acid), in the pathophysiology of posthypoxic myoclonus were investigated. Administration of guvacine (1 or 10 mg/kg, IP) or nipecotic acid (0.5 or 5 mg/kg, IP) significantly attenuated myoclonus scores of the animals. Tolerance to antimyoclonus effects of these two compounds did not develop after chronic administration (twice a day for 14 days) of guvacine (10 mg/kg, IP) or nipecotic acid (5 mg/kg, IP). On the other hand, tolerance was noticed with clonazepam (2.5 mg/kg, IP twice a day for 7 days). The results indicate that guvacine or nipecotic acid may be used in combination with (at reduced doses) or as alternatives to clonazepam to treat patients with the disease so as to reduce tolerance phenomenon usually associated with clonazepam.

Animals↗
PubMed1994

Progressive decrease in extracellular GABA concentrations in the post-ischemic period in the striatum: a microdialysis study.

Repetitive cerebral ischemia in gerbils produces delayed neuronal damage in the substantia nigra reticulata (SNr). This damage begins 4 to 5 days after the insult and is severe by day 7. The damage can be attenuated by GABA agonists. There is a prominent GABAergic striatal pathway to the SNr. Damage to this pathway leads to progressive loss of SNr neurons. This loss can be prevented by GABA agonists. We postulate that, ischemia-induced lack of GABAergic inhibitory input from the striatum to the SNr, may be responsible for this delayed neuronal damage. In the present experiment, we have measured striatal extracellular GABA concentrations with or without nipecotic acid, a GABA-reuptake inhibitor, in gerbils exposed to repetitive ischemia. GABA levels were measured on days 1, 3, 5, and 7 after the ischemic insult. Five control animals and a similar number of ischemic animals were monitored on each day. Extracellular fluid was collected using in vivo microdialysis and GABA levels were measured by electrochemical detection with HPLC. The extracellular striatal GABA levels were very low in the initial three specimens collected, both in the control and in the ischemic animals. However, addition of nipecotic acid resulted in an immediate increase of GABA in measurable range. In comparison to the controls, the increase in GABA on day 1 and 3 were significantly higher in animals with repetitive ischemia (two-way ANOVA with repeated measures). Subsequent measurements showed a gradual decrease in GABA levels when compared to controls. The increase in GABA with nipecotic acid was significantly lower on day 7 after the ischemic insults when compared to the controls. The increased GABA responsiveness immediately after the ischemic insults may reflect a protective effect against excitotoxicity. The subsequent decline in GABA levels after the insult may be secondary to progressive loss of striatal GABAergic neurons. This may contribute to the production of delayed neural damage in the SNr by a decrease in the inhibitory striatal input.

Animals↗
PubMed1989

On the origin of extracellular GABA collected by brain microdialysis and assayed by a simplified on-line method.

The present study describes a simplified on-line system for determination of GABA in brain dialysates. GABA was determined with an isocratic HPLC method after derivatization with o-phthaldialdehyde. One peristaltic pump was sufficient to transport both the perfusion fluid and the derivatizing reagent. The basal release of GABA was stimulated by infusion with either elevated K+ or the GABA uptake inhibitor (-)-nipecotic acid. Basal as well as stimulated GABA release were investigated for possible calcium-dependency by infusing submmolar amounts of the potent calcium antagonist cadmium. Infusion of cadmium did not modify the dialysate concentrations of GABA. In addition basal as well as nipecotic acid enhanced release of GABA dialysate concentrations were investigated for nerve-impulse dependency by infusing mumolar amounts of tetrodotoxin. No change in the GABA output was observed during infusion of TTX. From these results it is concluded that the basal as well as the nipecotic acid induced release of GABA did not fulfill the criteria for classic exocytotic release. Possible explanations for these unexpected findings are discussed.

Animals↗
PubMed1989

gamma-Aminobutyric acid uptake and localization in bovine chromaffin cells in primary culture.

gamma-Aminobutyric acid (GABA) uptake was studied in bovine chromaffin cells maintained in primary culture. Uptake was found to be dependent on Na+, but not on K+ and Ca2+ ions; it was found that 2 Na+ ions were necessary for each molecule of GABA transported. 2,4-Dinitrophenol, ouabain and vanadate inhibited GABA uptake showing the energy dependency of the system. Two affinity sites were demonstrated, a high affinity site and a low affinity site with Km values of 10 microM and 170 microM, respectively. While the low affinity site did not show large variations with culture age, the Km of the high affinity site increased from 1 microM in freshly isolated cells to 10 microM in 3-9 day-old cells. GABA uptake was unaffected by glutamic acid, aspartic acid, glycine and catecholamines, while taurine, beta-alanine, nipecotic acid and L-2,4 diaminobutyric acid inhibited GABA uptake. Nipecotic acid and L-2,4 diaminobutyric acid acted as competitive inhibitors modifying Km values of the high affinity site. Subcellular studies performed on [3H]GABA-loaded chromaffin cells showed that GABA was not in secretory granules but was recovered in the 100,000 g soluble fraction. The GABA uptake process associated with chromaffin cells may be an important mechanism for regulating the modulation of catecholamine secretion. In addition, the presence of GABA in the cytosol indicates that this molecule may be an effector of chromaffin cell activity in addition to modulating catecholamine secretion.

Adrenal Medulla↗
PubMed2005

Production of novel rapamycin analogs by precursor-directed biosynthesis.

The natural product rapamycin, produced during fermentation by Streptomyces hygroscopicus, is known for its potent antifungal, immunosuppressive, and anticancer activities. During rapamycin biosynthesis, the amino acid l-pipecolate is incorporated into the rapamycin molecule. We investigated the use of precursor-directed biosynthesis to create new rapamycin analogs by substitution of unusual l-pipecolate analogs in place of the normal amino acid. Our results suggest that the l-pipecolate analog (+/-)-nipecotic acid inhibits the biosynthesis of l-pipecolate, thereby limiting the availability of this molecule for rapamycin biosynthesis. We used (+/-)-nipecotic acid in our precursor-directed biosynthesis studies to reduce l-pipecolate availability and thereby enhance the incorporation of other pipecolate analogs into the rapamycin molecule. We describe here the use of this method for production of two new sulfur-containing rapamycin analogs, 20-thiarapamycin and 15-deoxo-19-sulfoxylrapamycin, and report measurement of their binding to FKBP12.

Biotechnology↗
PubMed1997

GABA uptake sites in frontal cortex from suicide victims and in aging.

The binding of [3H]nipecotic acid to GABA uptake sites was studied in post mortem human frontal cortex from 17 suicide victims and 21 controls without known neurological or psychiatric disorder. The suicide victims were subclassified according to the use of violent or non-violent methods and to the presence or absence of a known history of a depressive disorder. No difference was found between the suicide victims and the controls with regard to [3H]nipecotic acid binding to GABA uptake sites (Bmax) and apparent affinity (Kd). No differences were found either with regard to method of suicide or whether a depressive symptom existed or not. The binding of [3H]nipecotic acid to GABA uptake sites was also studied in post mortem human frontal cortex with regard to aging. The age of the subjects ranged from 16 to 84 years. No significant difference in either Bmax or Kd was found. The present findings suggest that the GABA uptake sites in the human frontal cortex are not subjected to regulation or degenerative changes in conditions investigated.

Aged↗
PubMed1995

Further evidence for the interactions between angiotensin II and GABAergic transmission in pentylenetetrazol kindling seizures in mice.

The effects of the GABAergic drugs nipecotic acid, Gabrene, baclofen and metatolylcarbamide (MTC), when given alone or in combination at subthreshold doses with AT II also at a subthreshold dose effective on PTZ-kindling in mice were studied. PTZ-kindling was provoked by intraperitoneal (i.p.) injections of PTZ (40 mg/kg) every other day in male albino mice until clonic seizures appeared. Nipecotic acid (100 and 200 micrograms/mouse intracerebroventricularly [i.c.v.]) tended to decrease seizure intensity. Gabrene (25, 50, 100 and 250 mg/kg i.p.) inhibited PTZ-kindled seizures. Baclofen at a doses of 2.5 and 5 mg/kg i.p. tended to decrease seizure intensity and at a dose of 10 mg/kg was ineffective at all. MTC (50 and 75 mg/kg i.p.) tended to decrease and at a dose of 100 mg/kg significantly decreased seizure intensity. Combinations of subthreshold dose of AT II (0.05 micrograms/mouse i.c.v.) and subthreshold doses of nipecotic acid (100 micrograms/mouse) or Gabrene (10 mg/kg) or baclofen (10 mg/kg) or MTC (50 mg/kg) significantly decreased the intensity of PTZ-kindled seizures in mice. The observed potentiation of the anticonvulsive activity on PTZ-kindling suggests interactions of AT II receptors with GABA receptors (GABAA, GABAB or both), effected through allosteric mechanisms.

Angiotensin II↗
PubMed1987

Adaptation of the GABAA-receptor complex in rat brain during chronic elevation of GABA by ethanolamine O-sulphate.

Slice preparations of rat cuneate nucleus were used for studies on the gamma-aminobutyric acid GABAA-receptor complex following chronic and acute pretreatment with GABA-alpha-ketoglutarate aminotransferase (GABA-T) inhibitors. The whole brain GABA concentration was significantly increased 2.9 fold and 2.6 fold following treatment with ethanolamine O-sulphate (EOS, orally) for 15-30 days and 56-64 days, respectively. One hour after a single injection of gamma-acetylenic GABA (GAG) i.p., there was a significant 2.1 fold increase in whole brain GABA. Superfusion of a slice with muscimol or the GABA uptake inhibitor nipecotic acid depolarized the afferent nerve fibres. These effects were potentiated by flurazepam (1 microM) and pentobarbitone (10 microM) and antagonized by picrotoxin (3 microM, 30 microM). Following 15-30 days of EOS-treatment, the depolarization response to muscimol was decreased and that to nipecotic acid increased. These changes were no longer significant by 56-64 days of pretreatment. The acute dose of GAG did not affect the depolarization response to muscimol but increased that to nipecotic acid. The potentiations of muscimol by flurazepam (1 microM) and pentobarbitone (10 microM) were enhanced following chronic EOS treatment (15-64 days). The enhancement of flurazepam was less after 56-64 days than after 15-30 days pretreatment whereas the enhancement of pentobarbitone was similar at both times. Acute GAG treatment had no effect. The potency of picrotoxin as an antagonist of muscimol was reduced following chronic EOS treatment; the enhancement was less after 56-64 days than after 15-30 days pretreatment. Acute GAG treatment caused only a very small reduction in picrotoxin potency. Possible adaptations in the GABAA-receptor complex and its modulation during chronic elevation of brain GABA are discussed.

4-Aminobutyrate Transaminase↗
PubMed1990

Effect of local inhibition of gamma-aminobutyric acid uptake in the dorsomedial hypothalamus on extracellular levels of gamma-aminobutyric acid and on stress-induced tachycardia: a study using microdialysis.

Previous studies involving local microinjection of drugs that interfere with gamma-aminobutyric acid (GABA)A receptor-mediated synaptic inhibition have led to the suggestion that endogenous GABA suppresses the activity of a sympatho-excitatory mechanism in the dorsomedial hypothalamus in rats. In this study, microdialysis was used to assess and to alter pharmacologically extracellular-levels of GABA within this region while simultaneously monitoring heart rate and blood pressure. In anesthetized rats, local microdialysis for 15 min with 2.5, 10 and 40 mM nipecotic acid, an inhibitor of GABA uptake, caused concentration-related increases in GABA and taurine in the extracellular space, but no significant change in heart rate or arterial pressure. Similar perfusion with 37.5, 75 and 150 mM KCl caused concentration-related increases in GABA as well as aspartate, glutamate, taurine, glycine and alanine. Only modest, variable increases in heart rate and no effect on arterial pressure were observed during the perfusions with high potassium. In conscious rats, unilateral microdialysis of the dorsomedial hypothalamus with 0.5 mM nipecotic acid for 2 to 2.5 hr before stress coupled with contralateral microinjection of muscimol (88 pmol/250 nl) 5 min before stress significantly reduced air stress-induced tachycardia; this reduction in tachycardia was associated with markedly elevated levels of GABA in dialysates collected from the dorsomedial hypothalamus. Neither treatment alone significantly influenced stress-induced increases in heart rate, although perfusion with nipecotic acid alone evoked similar elevations in extracellular GABA. These results suggest that extracellular levels of endogenous GABA in the dorsomedial hypothalamus may regulate the cardiovascular response to stress.

Amino Acids↗
PubMed2006

Neuropharmacological profile of FrPbAII, purified from the venom of the social spider Parawixia bistriata (Araneae, Araneidae), in Wistar rats.

The aims of the present study were to investigate the anticonvulsant activity and behavioral toxicity of FrPbAII using freely moving Wistar rats. Moreover, the effectiveness of this compound against chemical convulsants was compared to that of the inhibitor of the GABAergic uptake, nipecotic acid. Our results show that FrPbAII was effective against seizures induced by the i.c.v. injection of pilocarpine (ED(50) = 0.05 microg/animal), picrotoxin (ED(50) = 0.02 microg/animal), kainic acid (ED(50) = 0.2 microg/animal) and the systemic administration of PTZ (ED(50) = 0.03 microg/animal). The anticonvulsant effect of FrPbAII differed from that of nipecotic acid in potency, as the doses needed to block the seizures were more than 10 folds lower. Toxicity assays revealed that in the rotarod, the toxic dose of the FrPbAII is 1.33 microg/animal, and the therapeutic indexes were calculated for each convulsant. Furthermore, the spontaneous locomotor activity of treated animals was not altered when compared to control animals but differed from the animals treated with nipecotic acid. Still, FrPbAII did not induce changes in any of the behavioral parameters analyzed. Finally, when tested for cognitive impairments in the Morris water maze, the i.c.v. injection of FrPbAII did not alter escape latencies of treated animals. These findings indicate that the novel GABA uptake inhibitor is a potent anticonvulsant with mild side-effects when administered to Wistar rats.

Animals↗
PubMed1990

Synthesis of fluorine-18 labeled GABA uptake inhibitors.

The first syntheses of fluorine-18 labeled inhibitors of GABA reuptake [(R,S)-1-[2-[4-[18F]fluorophenyl]phenyl]methoxyethyl]piperidine- 3-carboxylic acid, (R,S)-1-[2-[(4-[18F]trifluoromethyl)phenyl][(4- trifluoromethyl)phenyl]-methoxyethyl]piperidine-3-carboxylic acid] are described. These N-substituted nipecotic acid derivatives were prepared in no-carrier-added form by the condensation of the appropriately substituted [18F]benzhydryl chlorides (prepared in three steps from [18F]fluoride ion) with N-(2-hydroxyethyl)nipecotic acid ethyl ester, followed by ester hydrolysis. Overall radiochemical yields were 17-28% (corrected, 150 min synthesis time). A simple new method for synthesis of a [18F]trifluoromethyl group by the nucleophilic substitution of a bromodifluoromethyl substituent has also been developed.

Fluorine Radioisotopes↗