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 VOLUME Vol.05 Issue03 2025 

PAGE NO. 19-24 

DOI 10.37547/ajbspi/Volume05Issue03-05 

 
 
 
 

Safety assessment of the 4- (6-phenyl-7h - [1,2,4] triazolo 

[3,4-b] [1,3,4] thiadiazine-3- yl) -aniline compound and the 

effects of the substance on respiration and cardiac 

activity 
 

Rahimboev Suhrob Davlatyor o‘g‘li 

Institute of Chemistry of Plant Substances Academy of Sciences of Republic of Uzbekistan 

 

Sanoev Zafar Isomiddinovich 

Institute of Chemistry of Plant Substances Academy of Sciences of Republic of Uzbekistan 

 

Khamroyev Tolmas Tolibovich 

Institute of Chemistry of Plant Substances Academy of Sciences of Republic of Uzbekistan 

 

Abdinazarov Ibrokhimjon Tuychiyevich 

Institute of Chemistry of Plant Substances Academy of Sciences of Republic of Uzbekistan 

 

Rashidov Sohib Zamon o‘g‘li 

Institute of Chemistry of Plant Substances Academy of Sciences of Republic of Uzbekistan 

 

Ismoilova Dilnoza Safaraliyevna 

Institute of Chemistry of Plant Substances Academy of Sciences of Republic of Uzbekistan 

 

Elmuradov Burkhon 

Institute of Chemistry of Plant Substances Academy of Sciences of Republic of Uzbekistan 

 

Received: 28 January 2025; Accepted: 27 February 2025; Published: 25 March 2025 

 

Abstract: 4-(6-phenyl-7H-[1,2,4]-triazolo-[3,4-b] - [1,3,4] - thiadiazine-3- yl) - aniline compound belongs to the 
group of triazole derivatives, belongs to class IV low-toxic compounds in acute toxicity, and sodium belongs to the 
compounds of this group, taking into account the presence of Due to its ability to block ion channels, it can be 
concluded that the 1.0 mg/kg dose studied during the experiment led to bradycardia in exchange for a decrease 
in the activity of the sinus node, which is considered the main regulator of the first-order heart rhythm. 

 

Keywords: Acute toxicity, accumulation, number of breaths, blood pressure, cardiac activity, rhythm. 

 

Introduction: Epilepsy is a chronic disease that is 
accompanied by a violation of the functioning of the 
neurons of the central nervous system, characterized 
by seizures and loss of ES Hus in exchange for a 
dysbalance of the activity of the excitatory and 

inhibitory mediators of the brain [1, 2]. Over the past 
few decades, more than 20 new antiepileptic drugs 
have been created, including escarbazepine acetate 
[3], perampanel [4] and ezogabin [5]. However, a large 
percentage of the population does not achieve a stable 
anticonvulsant effect with monotherapy [6], and about 

 

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30% of patients have refractory epilepsy and require a 
combination of treatment [7, 8]. In addition, many 
antiepileptic drug drugs have serious side effects [9, 10] 
and need lifelong treatment. Therefore, the search for 
more selective and safer anticonvulsant agents is of 
particular interest. In the same point of view, several 
antiepileptic drugs of different approaches were 
studied for the development of [11-13]. The GAMK-A 
receptor is a major target for a number of 
therapeutically important drugs such as barbiturates, 
steroids, anesthetics, and benzodiazepines [14,15]. 
1,2,4-triazole derivatives have been found to exhibit 
many biological activities, including anticonvulsant [16, 
17], anti-fungal [18-20], neurotrophic heterocyclic 
activity [21-24], anti-inflammatory [25-27], and 
antibacterial [28-31], based on experiments. The 
molecular structure and bioactivity of commercially 
available antiepileptic drugs are spatially long 
hydrophobic domains (typically phenyl rings), 
hydrogen-binding domains, and electron-donor 
fragments, elements required for high anticonvulsant 
activity. In addition, various other compounds with a 
1,2,4-triazole moiety were found to have 
anticonvulsant properties in several animal models of 
epilepsy [32-35]. These findings prompted us to look 
for 1,2,4-triazole-based compounds with 
anticonvulsant activity and determine if the derived 
derivatives could act on the allosteric site of GABA-A 
receptors. The combination of 4-(6-phenyl-7h-
[1,2,4]triazolo[3,4-b][1,3,4]thiadiazine-3-yl) - aniline 
conditionally (D-286) has been studied for its overall 
pharmacological activities and effects on vital organs. 

METHODS 

4-(6-phenyl-7H-[1,2,4]triazolo[3,4-b][1,3,4]thiadiazine-
3- yl) is an aniline compound, with the substance twine-
80 as a solvent, ethaminal-sodium as a narcosis agent, 
aconitin substance for arrhythmia calling purposes, 
mass 18-24 g white mice, 180-220 g white rats, cat with 
a mass of 2.2 kg, ZOOMED IM-10 cardiomonitor, a 
Schiller cardiovit at-1 electrocardiograph device was 
used. Experiments were carried out in a room with 30-
60% air humidity, 400 Lux lighting at a temperature of 
15-250C. The substance was observed for 14 days after 
one administration. The compound was evaluated for 

acute toxicity in oral white mice, venous white rats, 
cumulative properties, effects on vital organ function, 
and effects on heart rhythm. The results obtained were 
processed using statistical methods. 

RESULTS AND DISCUSSIONS 

1, Experiments on acute toxicity of the 2,4-triazole 
derivative D-286 were performed in white mice by oral 
administration of twin-80, administered at a dose of 
500 mg/kg to a dose of 4,500 mg/kg to assess the 
resorbtive effect and the time of death. 

In acute toxicity experimental animals, rates are 
assessed from a dose of up to 100% mortality with 
significant changes in the body. Each group receives at 
least 6 experimental animals. Acute toxicity of the 
compound 4-(6-phenyl-7H-(1,2,4)-triazolo(3,4-b)-
(1,3,4)-thiadiazine-3-yl) - aniline (D-286) was studied in 
white mice by oral administration at a dose of 500 
mg/kg to 4,500 mg/kg. At a dose of 500-1000 mg/kg, no 
significant changes were observed in experimental 
animals. From a dose of 1500 mg/kg, general 
powerlessness, motion attenuation began to be 
observed. With an increase in dose at doses of 2000-
4500 mg/kg, tremor, tail reaction, sustained Tonico-
clonic seizures, and death began to be observed at 
intervals of 3-7 hours. The average death dose was 
LD50 = 2150 mg/kg. The compound D-286 was studied 
intravenously at a dose of 100-500 mg/kg in white rats 
with a mass of 170-230 g. From a dose of 300 mg/kg, 
death began to be observed in experimental animals 
due to respiratory failure, tremor, seizures. The results 
obtained were LD50=351.25 mg/kg when the average 
death dose was administered intravenously after 
statistical processing. 

Determination of cumulative property in the 
compound D-286, calculated from 1,2,4-triazole 
derivatives with high anti-seizure activity, in different 
proportions of the dose of LD50. It was carried out 
using the method proposed by R. K. Lim. No deaths 
were reported during the experiment and the 15-day 
follow-up period after the compounds were sent for 28 
days. The results obtained are shown in Table 1. 

 

Table 1. 

Assessment of cumulative effects of compounds with activity higher than 1,2,4-

triazole derivatives when administered orally in white mice 

Experience days 1-4 5-8 9-12 13-16 17-20 21-24 25-28 cumulative 

coefficient 

Cc 

LD50 share 0.1 0.15 0.22 0.34 0.5 0.75 1.12  



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Cc=27348/2150= 

12.72 

According to the results obtained, it turns out that the 
compound D-286 of the 1,2,4-triazole derivative does 
not have a cumulative property. 

The effect of drug substance on breathing and heart 
function. Study of the effect of D–286 on arterial blood 
pressure in a research setting. Studies investigating the 
effects of D-286 on arterial blood pressure were 
conducted on a ZOOMED IM-10 cardiomonitor, in cats 
with a body weight of 2.2 kg, the substance studied was 
sent to the intra-abdominal introduction at a dose of 
1.0 mg/kg. Prior to the experiments, preliminary 
indications demonstrated in cardiomonitor were 
recorded by calling narcosis using a cat's intra-
abdominal introduction 40 mg/kg dose of ethaminal 
sodium. In studies, arterial blood pressure was 
monitored for 2 hours, starting from 10 minutes of the 
experiment, and the indicators on the cardiomonitor 
were recorded. In this experiment, in addition to 

arterial blood pressure, indicators such as the number 
of heart contractions, body temperature, saturation 
were also recorded. As a result of the study carried out, 
it was assessed by the differences that occurred in 
relation to the initial indicators demonstrated on the 
cardiomonitor. In studies carried out, arterial blood 
pressure under the influence of a dose of 1.0 mg/kg of 
the D-286 compound was observed almost no changes 
in the oxygen saturation of hemoglobin i.e. saturation 
indicators. A decrease in body temperature at 1-1.5℃, 
a decrease in the number of breaths, as well as a return 
to the initial state after 2 hours can be seen. In contrast, 
the number of cardiac contractions can be seen to have 
increased compensatorically after initial narcosis from 
124 to 141 times, and later decreased experimentally 
from 135 to 94 times after administration of the 
studied substance, leading to bradycardia (Table 2). 

 

Table 2. 

The effect of D-286 on AQB, number of breaths and other indicators. 

№  Substance D-286 at a dose of 1.0 mg / kg 

Indicators studied in cardiomonitor 

The time when the 

observation was 

carried out in 

minutes 

Blood pressure in 

mmHg 

heart rate 

number 

Number 

of 

breaths 

Body 

temperature 

at ℃ 

Saturation in 

% 

1. Initial condition 125/83 124 12 37.6 87 

2. D-286 1.0 mg/kg 

10 minutes after 

administration 

113/46 141 11 37.6 87 

3. 20 114/57 135 9 36.9 85 

4. 30 121/80 130 8 36.3 85 

5. 40 126/71 121 8 36.8 85 

6. 50 119/66 114 8 36.6 84 

7. 60 119/66 113 8 36.5 86 

8. 70 123/76 111 8 36.1 85 

9. 80 118/76 105 7 36.8 86 

10. 90 125/83 104 7 36.6 85 

11. 100 135/79 100 7 36.7 85 

12. 120 133/78 98 9 36.8 86 



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13. 130 129/82 94 12 37.3 86 

Determination of the effect of the D-286 compound on 
cardiac electrophysiological indicators. The effect of 
the D-286 compound on the electrophysiological 
indicators of the heart scientific studies conducted in 
the study body weight 180-220 g. in laboratory white 
rats up to, SCHILLER CARDIOVIT was achieved by 
recording on the standard II connection of the AT-1 ECG 
hardware. For this purpose, the studied compound is 
evaluated for normal cardiac activity as well as 
antiarrhythmic activity in peripheral Genesis disorders 
of the heart rhythm through arrhythmia models called 
through a chemical compound of arrhythmic nature. 
Before the start of the experiment, an  

electrocardiogram (ECG) analysis was carried out on 
the standard connection II in animals, and after that 
aconitin was sent to the tail vein in rats with a dose of 
12-15 mcg/kg, which is called mixed in animals of all 
experimental groups-ventricular extrasystole. The 
formation of cardiac rhythm disturbances began in 1-2 
minutes after the cessation of administration of 
aconitin, based on the rule. Writing in EKG was 
conducted in 1; 3; 5; 10; 15 and 20 minutes after 
administration of aconitin. The substance under study 
was administered 60 minutes before oral aconitin 
administration at doses of 1.0; 10.0; 30.0 and 60.0 
mg/kg, and at doses of 1.0; 2.0 and 10.0 mg/kg after 
arrhythmia caused by aconitin. All the experiments 
carried out were carried out in accordance with the 
Control Research Scheme. The activity of the studied 
compound was assessed by its prevention of heart 
rhythm disturbances called aconitin. 

Initially, the compound D-286 was used through the 
above-mentioned dosages and injection methods, the 
changes caused by its action on the normative 
electrophysiological indicators of the heart were 
recorded in the II standard connection of the ECG for 
60-70 minutes after the introduction of the substance. 
When the D-286 compound was administered orally at 
doses of 1.0; 10.0; 30.0 and 60.0 mg/kg, it was observed 
that the number of heart contractions in 50-60 minutes 
of the study decreased by an average of 30-35 times 
compared to the original. No changes were observed in 
pqrst tooth voltage, with the intervals of PQ(R) and QRS 
(T) extending by 4-6% compared to the original. These 
results obtained indicate a decrease or slowdown in 
cardiac AV and Inter-ventricular conduction under the 
influence of the studied substance. 

It was observed that the substance studied showed 
anti-arrhythmia activity called by aconitin, 
corresponding to each dose, when administered orally 
at the doses noted above. Heart rhythm disturbances  

in the form of polyphocals associated with cardiac 
conduction disorders occurred in the first minute after 
the introduction of aconitin at a dose of 1.0 mg/kg, and 
symptoms of recovery began to occur in these rhythm 
disturbances, which occurred from 11 minutes of the 
study, and a complete recovery of the rhythm was 
observed in 20-25 minutes. With aconitin exposure at 
doses of 10.0; 30.0 and 60.0 mg/kg, heart rhythm 
disturbances in the form of polyphocals occurred at 
4.0; 2.0 and 1.5 minutes of the study, respectively, and 
from 10; 13 and 15 minutes began to develop signs of 
a begging of a disturbed rhythm. At a dose of 10 mg/kg, 
after 10 minutes of the study, the broken rhythm was 
completely restored according to all indicators, while at 
a dose of 30 mg/kg it was restored after 18 minutes, at 
a dose of 60 mg/kg, the rhythm recovery time was 5 
minutes.Also, rhythm disturbances caused by aconitin 
exposure when the substance studied was injected 
intravenously for treatment purposes-from 3-4 
minutes of the study under the action of a dose of 1.0 
mg/kg-to the recovery of the disturbed rhythm-this 
rhythm recovery took up to 8-10 minutes. Signs of 
recovery of rhythm disturbances caused by aconitin 
exposure at doses of 2.0 and 10.0 mg/kg began to occur 
from 5 and 11 minutes of the study, and a complete 
recovery of rhythm occurred at 10 and 16 minutes. 

CONCLUSION 

Thus, the compound 4-(6-phenyl-7H-[1,2,4]-triazolo-
[3,4-b]-[1,3,4]-thiadiazine-3-yl)-aniline belongs to the 
group of triazole derivatives, according to Stefanov on 
acute toxicity, class IV is among the less toxic 
compounds, and considering the presence of the 
sodium ion channel blocking property among these 
group compounds, the sinus, which was considered the 
first-order main controller of heart rhythm at a dose of 
1.0 mg/kg studied during the experiment it can be 
concluded that nodini caused bradycardia in exchange 
for decreased activity. Although few signs of 
bradycardia occur under the influence of the 
substance, it does not negatively affect the normative 
electrophysiological indicators of the heart. In addition, 
in cardiac arrhythmias called by aconitin, its activity 
against arrhythmias can be associated with the siege of 
Na+ channels. 

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