Haloperidol: Discovery, Structure and Mechanisms

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8th Feb 2020 Chemistry Reference this

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Haloperidol

Discovery

Haloperidol was firstly discovered in 1958 in Belgium by a scientist named Bert Hermans within the Janssen Pharmaceutical Company. The drug was initially piloted on mice to observe any such effects on their state of excitability. Haloperidol contributed promising results and caused the mice to become placid post administration. Psychiatrists Divry, Bobon and Collard first administered the drug to humans in the Liege Hospital, Belgium where the findings led to the neuroleptic able to facilitate the discharge of chronic patients under regular dosage (Granger, 1999). Due to the success of these combined findings Haloperidol was granted the go ahead for licencing and was first marketed in Belgium in October of 1959. Today, haloperidol is a widely prescribed drug used mainly in the treatment of acute psychosis and schizophrenia and has been granted a place on the World Health Organisation’s list of essential medicines (López-Muñoz and Alamo, 2009).

Structure, Class and Associated physiochemical properties

Haloperidol has the structure of a phenyl-piperidinyl-butyrophenone as depicted in Figure 1 below.

 

Figure 1 to show the chemical structure of Haloperidol (PubChem, 2018).

Haloperidol is classed as a typical anti-psychotic drug which falls under the phenothiazines chemical class with the inclusion of a piperazine side chain (Battista, Page and Horton-Szar, 2015).

Haloperidol is a white/ faint yellow odourless amorphous/ microcrystalline powder which is practically insoluble in water. The molecular formula for haloperidol is C21H23C1FNO2 and it has a molecular weight of 375.9. It is considered under the structural chemical names; 4-[4-(4-Chlorophenyl)-4-hydroxypiperidino]-4′- fluorobutyrophenone, 4[4-(4-Chlorophenyl)-4-hydroxy-1-piperidinyl]-1-(4-fluorophenyl)-1-butanone and 4[4-(p-Chlorophenyl)-4-hydroxypiperidino]-4′-fluorobutyrophenone (Higa de Landoni, 2018).

Principal mechanism of action including drug-target interactions

Haloperidol’s mechanism of action is not yet completely understood, however it is established that it hinders the effects of the neurotransmitter dopamine and increases its metabolism in the body (Drugbank.ca, 2018).

Dopamine binds to a D2 receptor where it can induce a change on the body. Its main role includes transmitting signals between neurons (Newton, 2018). Dopamine over activity can be observed at either pre or post synaptic locations of the synaptic cleft. Pre synaptic over activity is seen by excess dopamine release by the dopamine nerve terminals. Post synaptic over activity is seen by an increase in the number of D2 receptors or post-receptor action.  

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Haloperidol interacts with dopamine by binding to the dopamine D2 receptor at a higher affinity than dopamine itself. It also has a dissociation constant lower than that of dopamine, meaning it can stay bound to the receptor for longer (Drugbank.ca, 2018).

Haloperidol works to treat the effects of psychosis by competitively blocking the post-synaptic D2 receptors in the brain. This halts dopamine neurotransmission which relieves delusions and hallucinations which are commonly experienced by psychosis patients (Maddison, Page and Church, 2009). Approximately 60-80% of D2 receptors in the brain can be inhibited through haloperidol’s blocking effect, meaning it is an effective drug (Drugbank.ca, 2018).

Although Haloperidol is an effective antipsychotic drug it can cause serious side effects, namely extrapyramidal symptoms (EPS). This is induced by the intensity of the bond between the drug and the D2 receptor. Sometimes these symptoms can last for the lifetime of the patient (Drugbank.ca, 2018).

In order to combat these EPS a modified class of antipsychotic drugs were developed. There are referred to as atypical drugs, e.g. olanzapine. Atypical drugs have a much lower risk of inducing EPS. These drugs differ from typical drugs such as haloperidol by rapidly dissociating from dopamine D2 receptors and binding at a lower affinity (Drugbank.ca, 2018).

CYP3A4 is the main isoform involved in the metabolism of haloperidol. Haloperidol acts as a substrate for CYP3A4 and an inhibitor as well as a stimulator of CYP2D6. Reduced haloperidol has a similar effect but does not stimulate CYP2D6. It is suggested that the variability in hepatic and intestinal CYP3A4 activity is the main cause of patients differing reactions to haloperidol (Shoji Kudo, 1999).

ADME

Haloperidol can either be administered orally or by intravenous injection. It is absorbed well in the gastrointestinal tract after oral ingestion. However, a small amount of the drug is metabolised by the liver before it can be circulated throughout the body. This is known as the hepatic first pass effect, which reduces the oral bioavailability of the drug to between 40-70% (Drugbank.ca, 2018). When administered intravenously, haloperidol has a 100% bioavailability (Mandal, 2018).

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The plasma concentration of haloperidol rises gradually with time and peaks around 6 days after absorption. The serum concentration can peak from 30 minutes to 4 hours after oral ingestion. Haloperidol’s half-life is around 21 days (de Leon et al., 2004).

After ingestion, haloperidol is spread throughout the body with high concentrations within the adipose tissue. 90% of haloperidol in the body is bound to proteins which are easily distributed around the body (Mandal, 2018).

Haloperidol is primarily metabolised by the liver through the process of glucuronidation (50-60%) where it is broken down extensively. This is followed by reduction of haloperidol to reduced hydroxyhaloperidol which accounts for 25% of metabolism. The remaining 15-30% is metabolised by oxidative N-dealkylation and pyridinium formation (Thorn, 2018).

Approximately 40% of each dose of haloperidol is excreted in the urine within 5 days of administration. Approximately 15% is excreted in the faeces. 1% of the drug will remain unchanged at the point of excretion (Drugbank.ca, 2018).

Toxicology and contraindications

Extrapyramidal reactions occur frequently with haloperidol due to its long half-life it is more likely to reach toxic levels within the body. If toxic levels are reached Tardive Dyskinesias (TDs) are likely to be displayed. These consist of involuntary, dyskinetic movements of the tongue, lips, face, trunk, and extremities which could potentially be irreversible. TDs are especially common in elderly women. Haloperidol is able to induce TDs by inflicting neuronal damage through an oxidative mechanism which encourages the production of free radicals through the mitochondria (Lohr, Kuczenski and Niculescu, 2003). There are no known treatments for established cases of tardive dyskinesia (Drugbank.ca, 2018).

Administration of haloperidol is strongly discouraged altogether for patients who have previous experience of strokes, comas or heart disease. Due to the psychological nature of psychosis and conditions associated with it, it is advisable not to administer haloperidol to any patient who is involved with any drug which could act as a central nervous system depressant, such as alcohol and caffeine (Cherry, 2018).

Patients who have previous incidence of Parkinson’s disease or dementia with Lewy bodies, aren’t advised not to take haloperidol but are encouraged to show special consideration when taking it (Ananya Mandal, 2018). If the patient is epileptic, haloperidol can increase the likelihood of convulsion occurring. Strong warning is given to patients with hyperthyroidism as haloperidol’s effects are seen more strongly and there is an increased risk of developing side effects. Patients with impaired liver function also respond differently to haloperidol as the liver is the main site of metabolism. Patients with QT prolongation are at a higher risk of arrhythmia originating within the ventricles (FDA, 2005)

Latest research advances

A recent study conducted by McGill University and the German Cancer Research Centre concluded that haloperidol was able to slow tumour growth and metastatic spread when tested on mice. The D2 receptor promotes growth and spread of pancreatic cancer. Haloperidol was able to combat this by blocking the function of this receptor. Blocking the dopamine receptor inhibits cancer growth and since haloperidol binds to the receptors tightly and with such high affinity it was an effective treatment. The researchers planted human pancreatic cancer cells into mice. The tumours were allowed to develop and grow. When treated with haloperidol it was concluded that haloperidol decreased the size of the tumours and fewer metastases occurred than untreated mice (Jandaghi et al., 2016).

A second study shows the effect of chronic exposure of haloperidol on the genes that play a critical role in myelin/oligodendrocyte function. This study was conducted on mice and looked at their brains. They concluded that there is a strong evidence the signalling pathways in oligodendrocytes are affected by haloperidol. This demonstrates that haloperidol has a specific effect on the myelin/oligodendrocyte genes (Narayan, Kass and Thomas, 2007).

References

  • Battista, E., Page, C. and Horton-Szar, D. (2015). Crash Course: Pharmacology. 4th ed. London: Mosby Elsevier, pp.82,83.
  • López-Muñoz, F. and Alamo, C. (2009). The consolidation of neuroleptic therapy: Janssen, the discovery of haloperidol and its introduction into clinical practice. PubMed. [online] Available at: https://www.ncbi.nlm.nih.gov/pubmed/19186209 [Accessed 17 Oct. 2018].
  • Granger, B. (1998). The discovery of haloperidol. PubMed. [online] Available at: https://www.ncbi.nlm.nih.gov/pubmed/10205735 [Accessed 17 Oct. 2018].
  • PubChem (2018). Haloperidol Chemical Structure. [image] Available at: https://pubchem.ncbi.nlm.nih.gov [Accessed 17 Oct. 2018].
  • Higa de Landoni, J. (2018). [online] Available at: http://www.inchem.org/documents/pims/pharm/haloperi.htm#PartTitle:3.%20PHYSICO-CHEMICAL%20PROPERTIES [Accessed 17 Oct. 2018].
  • De Leon, J., Diaz, F., Wedlund, P., Josiassen, R., Cooper, T. and Simpson, G. (2004). Haloperidol Half-life After Chronic Dosing. Journal of Clinical Psychopharmacology, [online] 24(6), pp.656-660. Available at: https://www.ncbi.nlm.nih.gov/pubmed/15538130 [Accessed 20 Nov. 2018].
  • Drugbank.ca. (2018). Haloperidol – DrugBank. [online] Available at: https://www.drugbank.ca/drugs/DB00502 [Accessed 21 Nov. 2018].
  • Newton, P. (2018). What is dopamine?. [online] Psychology Today. Available at: https://www.psychologytoday.com/us/blog/mouse-man/200904/what-is-dopamine [Accessed 21 Nov. 2018].
  • Maddison, J., Page, S. and Church, D. (2009). Small animal clinical pharmacology. 1st ed. Edinburgh: Saunders Elsevier, pp.126-147.
  • Cherry, K. (2018). How Depressants Affect Your Body. [online] Verywell Mind. Available at: https://www.verywellmind.com/what-are-depressants-2795572 [Accessed 22 Nov. 2018].
  • Ananya Mandal, M. (2018). Haloperidol Pharmacokinetics. [online] News-Medical.net. Available at: https://www.news-medical.net/health/Haloperidol-Pharmacokinetics.aspx [Accessed 16 Nov. 2018].
  • FDA. (2005). Halodol 1st ed. [pdf] Ortho-McNeil Pharmaceutical, Inc., pp.1-13. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/015923s082,018701s057lbl.pdf [Accessed 22 Nov. 2018].
  • Lohr, J., Kuczenski, R. and Niculescu, A. (2003). Oxidative Mechanisms and Tardive Dyskinesia. [online] PubMed. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12467492 [Accessed 22 Nov. 2018].
  • Shoji Kudo, T. Ishizaki., 1999. Pharmacokinetics of Haloperidol. Clinical Pharmacokinetics, 37(6), pp. 435-456. Available at: https://link.springer.com/article/10.2165/00003088-199937060-00001 [Accessed 22 Nov. 2018].
  • Jandaghi, P., Najafabadi, H., Bauer, A., Papadakis, A., Fassan, M., Hall, A., Monast, A., von Knebel Doeberitz, M., Neoptolemos, J., Costello, E., Greenhalf, W., Scarpa, A., Sipos, B., Auld, D., Lathrop, M., Park, M., Büchler, M., Strobel, O., Hackert, T., Giese, N., Zogopoulos, G., Sangwan, V., Huang, S., Riazalhosseini, Y. and Hoheisel, J. (2016). Expression of DRD2 Is Increased in Human Pancreatic Ductal Adenocarcinoma and Inhibitors Slow Tumor Growth in Mice. Gastroenterology, [online] 151(6), pp.1218-1231. Available at: https://www.sciencedirect.com/science/article/pii/S0016508516349824 [Accessed 22 Nov. 2018].
  • Narayan, S., Kass, K. and Thomas, E. (2007). Chronic haloperidol treatment results in a decrease in the expression of myelin/oligodendrocyte-related genes in the mouse brain. Journal of Neuroscience Research, [online] 85(4), pp.757-765. Available at: https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.21161 [Accessed 22 Nov. 2018].

Critical assessment

The aim of this assignment was to produce a report on my allocated anti-schizophrenic drug, Haloperidol. The report was to be aimed towards the non-scientific reader and was to fall between 1200-1400 words. The report was to be referenced using Harvard style citations and to be written using the aid of peer reviewed material such as journals and books. I used a combination of both of these sources with frequent references to PubMed, Google Scholar and well renowned organisations such as the Food and Drug Administration (FDA). It was important to source accurate and recent information which still has relevance today. My report was divided into sections, each covering a topic of information which would be valuable to grasp a full understanding of Haloperidol and its clinical uses. Following this structure allowed the report to flow between headings and guide the reader through the information clearly section by section. To improve my report I could have added more diagrams to break up the text in an attempt to better engage the non-scientific reader. However I believe I delivered the information in a simple and concise format which should be easily understood. I also struggled to find recent information as my drug is within the typical class which has since been improved and the atypical class is now preferred.

Reflective account

I believe this assignment has been a valuable foresight into the types of tasks likely to be encountered within the workplace. The skills acquired include, conveying a piece of information concisely whilst adhering to a word limit and writing for a non-specialised audience, meaning each point had to be explained simply which tested my own understanding of the content I was producing. These are two very important skills which are transferable to a vast amount of career paths, not only those of scientific origin. Independent study is another skill necessary for this task which will be expected by an employer when they set tasks to be done within the workplace. Adhering to a deadline is undoubtedly a skill necessary for every career which was also tested by this task. Producing your own content based upon others and discerning which information is relevant and which should be disregarded is also a skill which has been displayed. Having minimal instructions as to how the content should be delivered also tested our own initiative as to how to produce the report. I learned the importance of fully grasping an understanding of how Haloperidol works and why it was necessary to develop an atypical class of drug to improve upon its specific mechanisms. Accurate spelling, punctuation and grammar was vital to this task and conscientious referral to the word limit for each heading was imperative to achieve the overall 1200-1400 target.

Haloperidol

Discovery

Haloperidol was firstly discovered in 1958 in Belgium by a scientist named Bert Hermans within the Janssen Pharmaceutical Company. The drug was initially piloted on mice to observe any such effects on their state of excitability. Haloperidol contributed promising results and caused the mice to become placid post administration. Psychiatrists Divry, Bobon and Collard first administered the drug to humans in the Liege Hospital, Belgium where the findings led to the neuroleptic able to facilitate the discharge of chronic patients under regular dosage (Granger, 1999). Due to the success of these combined findings Haloperidol was granted the go ahead for licencing and was first marketed in Belgium in October of 1959. Today, haloperidol is a widely prescribed drug used mainly in the treatment of acute psychosis and schizophrenia and has been granted a place on the World Health Organisation’s list of essential medicines (López-Muñoz and Alamo, 2009).

Structure, Class and Associated physiochemical properties

Haloperidol has the structure of a phenyl-piperidinyl-butyrophenone as depicted in Figure 1 below.

 

Figure 1 to show the chemical structure of Haloperidol (PubChem, 2018).

Haloperidol is classed as a typical anti-psychotic drug which falls under the phenothiazines chemical class with the inclusion of a piperazine side chain (Battista, Page and Horton-Szar, 2015).

Haloperidol is a white/ faint yellow odourless amorphous/ microcrystalline powder which is practically insoluble in water. The molecular formula for haloperidol is C21H23C1FNO2 and it has a molecular weight of 375.9. It is considered under the structural chemical names; 4-[4-(4-Chlorophenyl)-4-hydroxypiperidino]-4′- fluorobutyrophenone, 4[4-(4-Chlorophenyl)-4-hydroxy-1-piperidinyl]-1-(4-fluorophenyl)-1-butanone and 4[4-(p-Chlorophenyl)-4-hydroxypiperidino]-4′-fluorobutyrophenone (Higa de Landoni, 2018).

Principal mechanism of action including drug-target interactions

Haloperidol’s mechanism of action is not yet completely understood, however it is established that it hinders the effects of the neurotransmitter dopamine and increases its metabolism in the body (Drugbank.ca, 2018).

Dopamine binds to a D2 receptor where it can induce a change on the body. Its main role includes transmitting signals between neurons (Newton, 2018). Dopamine over activity can be observed at either pre or post synaptic locations of the synaptic cleft. Pre synaptic over activity is seen by excess dopamine release by the dopamine nerve terminals. Post synaptic over activity is seen by an increase in the number of D2 receptors or post-receptor action.  

Haloperidol interacts with dopamine by binding to the dopamine D2 receptor at a higher affinity than dopamine itself. It also has a dissociation constant lower than that of dopamine, meaning it can stay bound to the receptor for longer (Drugbank.ca, 2018).

Haloperidol works to treat the effects of psychosis by competitively blocking the post-synaptic D2 receptors in the brain. This halts dopamine neurotransmission which relieves delusions and hallucinations which are commonly experienced by psychosis patients (Maddison, Page and Church, 2009). Approximately 60-80% of D2 receptors in the brain can be inhibited through haloperidol’s blocking effect, meaning it is an effective drug (Drugbank.ca, 2018).

Although Haloperidol is an effective antipsychotic drug it can cause serious side effects, namely extrapyramidal symptoms (EPS). This is induced by the intensity of the bond between the drug and the D2 receptor. Sometimes these symptoms can last for the lifetime of the patient (Drugbank.ca, 2018).

In order to combat these EPS a modified class of antipsychotic drugs were developed. There are referred to as atypical drugs, e.g. olanzapine. Atypical drugs have a much lower risk of inducing EPS. These drugs differ from typical drugs such as haloperidol by rapidly dissociating from dopamine D2 receptors and binding at a lower affinity (Drugbank.ca, 2018).

CYP3A4 is the main isoform involved in the metabolism of haloperidol. Haloperidol acts as a substrate for CYP3A4 and an inhibitor as well as a stimulator of CYP2D6. Reduced haloperidol has a similar effect but does not stimulate CYP2D6. It is suggested that the variability in hepatic and intestinal CYP3A4 activity is the main cause of patients differing reactions to haloperidol (Shoji Kudo, 1999).

ADME

Haloperidol can either be administered orally or by intravenous injection. It is absorbed well in the gastrointestinal tract after oral ingestion. However, a small amount of the drug is metabolised by the liver before it can be circulated throughout the body. This is known as the hepatic first pass effect, which reduces the oral bioavailability of the drug to between 40-70% (Drugbank.ca, 2018). When administered intravenously, haloperidol has a 100% bioavailability (Mandal, 2018).

The plasma concentration of haloperidol rises gradually with time and peaks around 6 days after absorption. The serum concentration can peak from 30 minutes to 4 hours after oral ingestion. Haloperidol’s half-life is around 21 days (de Leon et al., 2004).

After ingestion, haloperidol is spread throughout the body with high concentrations within the adipose tissue. 90% of haloperidol in the body is bound to proteins which are easily distributed around the body (Mandal, 2018).

Haloperidol is primarily metabolised by the liver through the process of glucuronidation (50-60%) where it is broken down extensively. This is followed by reduction of haloperidol to reduced hydroxyhaloperidol which accounts for 25% of metabolism. The remaining 15-30% is metabolised by oxidative N-dealkylation and pyridinium formation (Thorn, 2018).

Approximately 40% of each dose of haloperidol is excreted in the urine within 5 days of administration. Approximately 15% is excreted in the faeces. 1% of the drug will remain unchanged at the point of excretion (Drugbank.ca, 2018).

Toxicology and contraindications

Extrapyramidal reactions occur frequently with haloperidol due to its long half-life it is more likely to reach toxic levels within the body. If toxic levels are reached Tardive Dyskinesias (TDs) are likely to be displayed. These consist of involuntary, dyskinetic movements of the tongue, lips, face, trunk, and extremities which could potentially be irreversible. TDs are especially common in elderly women. Haloperidol is able to induce TDs by inflicting neuronal damage through an oxidative mechanism which encourages the production of free radicals through the mitochondria (Lohr, Kuczenski and Niculescu, 2003). There are no known treatments for established cases of tardive dyskinesia (Drugbank.ca, 2018).

Administration of haloperidol is strongly discouraged altogether for patients who have previous experience of strokes, comas or heart disease. Due to the psychological nature of psychosis and conditions associated with it, it is advisable not to administer haloperidol to any patient who is involved with any drug which could act as a central nervous system depressant, such as alcohol and caffeine (Cherry, 2018).

Patients who have previous incidence of Parkinson’s disease or dementia with Lewy bodies, aren’t advised not to take haloperidol but are encouraged to show special consideration when taking it (Ananya Mandal, 2018). If the patient is epileptic, haloperidol can increase the likelihood of convulsion occurring. Strong warning is given to patients with hyperthyroidism as haloperidol’s effects are seen more strongly and there is an increased risk of developing side effects. Patients with impaired liver function also respond differently to haloperidol as the liver is the main site of metabolism. Patients with QT prolongation are at a higher risk of arrhythmia originating within the ventricles (FDA, 2005)

Latest research advances

A recent study conducted by McGill University and the German Cancer Research Centre concluded that haloperidol was able to slow tumour growth and metastatic spread when tested on mice. The D2 receptor promotes growth and spread of pancreatic cancer. Haloperidol was able to combat this by blocking the function of this receptor. Blocking the dopamine receptor inhibits cancer growth and since haloperidol binds to the receptors tightly and with such high affinity it was an effective treatment. The researchers planted human pancreatic cancer cells into mice. The tumours were allowed to develop and grow. When treated with haloperidol it was concluded that haloperidol decreased the size of the tumours and fewer metastases occurred than untreated mice (Jandaghi et al., 2016).

A second study shows the effect of chronic exposure of haloperidol on the genes that play a critical role in myelin/oligodendrocyte function. This study was conducted on mice and looked at their brains. They concluded that there is a strong evidence the signalling pathways in oligodendrocytes are affected by haloperidol. This demonstrates that haloperidol has a specific effect on the myelin/oligodendrocyte genes (Narayan, Kass and Thomas, 2007).

References

  • Battista, E., Page, C. and Horton-Szar, D. (2015). Crash Course: Pharmacology. 4th ed. London: Mosby Elsevier, pp.82,83.
  • López-Muñoz, F. and Alamo, C. (2009). The consolidation of neuroleptic therapy: Janssen, the discovery of haloperidol and its introduction into clinical practice. PubMed. [online] Available at: https://www.ncbi.nlm.nih.gov/pubmed/19186209 [Accessed 17 Oct. 2018].
  • Granger, B. (1998). The discovery of haloperidol. PubMed. [online] Available at: https://www.ncbi.nlm.nih.gov/pubmed/10205735 [Accessed 17 Oct. 2018].
  • PubChem (2018). Haloperidol Chemical Structure. [image] Available at: https://pubchem.ncbi.nlm.nih.gov [Accessed 17 Oct. 2018].
  • Higa de Landoni, J. (2018). [online] Available at: http://www.inchem.org/documents/pims/pharm/haloperi.htm#PartTitle:3.%20PHYSICO-CHEMICAL%20PROPERTIES [Accessed 17 Oct. 2018].
  • De Leon, J., Diaz, F., Wedlund, P., Josiassen, R., Cooper, T. and Simpson, G. (2004). Haloperidol Half-life After Chronic Dosing. Journal of Clinical Psychopharmacology, [online] 24(6), pp.656-660. Available at: https://www.ncbi.nlm.nih.gov/pubmed/15538130 [Accessed 20 Nov. 2018].
  • Drugbank.ca. (2018). Haloperidol – DrugBank. [online] Available at: https://www.drugbank.ca/drugs/DB00502 [Accessed 21 Nov. 2018].
  • Newton, P. (2018). What is dopamine?. [online] Psychology Today. Available at: https://www.psychologytoday.com/us/blog/mouse-man/200904/what-is-dopamine [Accessed 21 Nov. 2018].
  • Maddison, J., Page, S. and Church, D. (2009). Small animal clinical pharmacology. 1st ed. Edinburgh: Saunders Elsevier, pp.126-147.
  • Cherry, K. (2018). How Depressants Affect Your Body. [online] Verywell Mind. Available at: https://www.verywellmind.com/what-are-depressants-2795572 [Accessed 22 Nov. 2018].
  • Ananya Mandal, M. (2018). Haloperidol Pharmacokinetics. [online] News-Medical.net. Available at: https://www.news-medical.net/health/Haloperidol-Pharmacokinetics.aspx [Accessed 16 Nov. 2018].
  • FDA. (2005). Halodol 1st ed. [pdf] Ortho-McNeil Pharmaceutical, Inc., pp.1-13. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/015923s082,018701s057lbl.pdf [Accessed 22 Nov. 2018].
  • Lohr, J., Kuczenski, R. and Niculescu, A. (2003). Oxidative Mechanisms and Tardive Dyskinesia. [online] PubMed. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12467492 [Accessed 22 Nov. 2018].
  • Shoji Kudo, T. Ishizaki., 1999. Pharmacokinetics of Haloperidol. Clinical Pharmacokinetics, 37(6), pp. 435-456. Available at: https://link.springer.com/article/10.2165/00003088-199937060-00001 [Accessed 22 Nov. 2018].
  • Jandaghi, P., Najafabadi, H., Bauer, A., Papadakis, A., Fassan, M., Hall, A., Monast, A., von Knebel Doeberitz, M., Neoptolemos, J., Costello, E., Greenhalf, W., Scarpa, A., Sipos, B., Auld, D., Lathrop, M., Park, M., Büchler, M., Strobel, O., Hackert, T., Giese, N., Zogopoulos, G., Sangwan, V., Huang, S., Riazalhosseini, Y. and Hoheisel, J. (2016). Expression of DRD2 Is Increased in Human Pancreatic Ductal Adenocarcinoma and Inhibitors Slow Tumor Growth in Mice. Gastroenterology, [online] 151(6), pp.1218-1231. Available at: https://www.sciencedirect.com/science/article/pii/S0016508516349824 [Accessed 22 Nov. 2018].
  • Narayan, S., Kass, K. and Thomas, E. (2007). Chronic haloperidol treatment results in a decrease in the expression of myelin/oligodendrocyte-related genes in the mouse brain. Journal of Neuroscience Research, [online] 85(4), pp.757-765. Available at: https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.21161 [Accessed 22 Nov. 2018].

Critical assessment

The aim of this assignment was to produce a report on my allocated anti-schizophrenic drug, Haloperidol. The report was to be aimed towards the non-scientific reader and was to fall between 1200-1400 words. The report was to be referenced using Harvard style citations and to be written using the aid of peer reviewed material such as journals and books. I used a combination of both of these sources with frequent references to PubMed, Google Scholar and well renowned organisations such as the Food and Drug Administration (FDA). It was important to source accurate and recent information which still has relevance today. My report was divided into sections, each covering a topic of information which would be valuable to grasp a full understanding of Haloperidol and its clinical uses. Following this structure allowed the report to flow between headings and guide the reader through the information clearly section by section. To improve my report I could have added more diagrams to break up the text in an attempt to better engage the non-scientific reader. However I believe I delivered the information in a simple and concise format which should be easily understood. I also struggled to find recent information as my drug is within the typical class which has since been improved and the atypical class is now preferred.

Reflective account

I believe this assignment has been a valuable foresight into the types of tasks likely to be encountered within the workplace. The skills acquired include, conveying a piece of information concisely whilst adhering to a word limit and writing for a non-specialised audience, meaning each point had to be explained simply which tested my own understanding of the content I was producing. These are two very important skills which are transferable to a vast amount of career paths, not only those of scientific origin. Independent study is another skill necessary for this task which will be expected by an employer when they set tasks to be done within the workplace. Adhering to a deadline is undoubtedly a skill necessary for every career which was also tested by this task. Producing your own content based upon others and discerning which information is relevant and which should be disregarded is also a skill which has been displayed. Having minimal instructions as to how the content should be delivered also tested our own initiative as to how to produce the report. I learned the importance of fully grasping an understanding of how Haloperidol works and why it was necessary to develop an atypical class of drug to improve upon its specific mechanisms. Accurate spelling, punctuation and grammar was vital to this task and conscientious referral to the word limit for each heading was imperative to achieve the overall 1200-1400 target.

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