BINDURA UNIVERSITY OF SCIENCE EDUCATION

Faculty of SCIENCE
CHEMISTRY DEPARTMENT

Student Name: FORTUNE MUNYARADZI VUSHE

REG No: B202612B
Course Code: CH205
Course Description: MEDICINAL CHEMISTRY
Lecturer: PROFESSOR DZOMBA
Program: CHEMICAL TECHNOLOGY
Level: 2.1
Assignment No: 1
1. Pharmaceutical effects occures when a ligand binds to a receptor. The section of the structure
of a ligand that binds to a receptor is known as its pharmacophore.
2.
(i) In-vitro analysis
The study of the effect of a drug on cells derived from an animal or a plant. The procedures are
done on cells outside their natural biological environment, such as in test tube or a laboratory
dish using artificial media to resemble biological fluids or the natural environment.
(ii) In-vivo analysis
The study of a drug in an animal when the whole animal is administered the drug. The
procedure is done directly inside or on a living body like an animal or a plant.
(iii) Clinical analysis
Are tests conducted on a drug to evaluate the effectiveness and safety of drugs by monitoring
their effects on large groups of people. Drugs are approved or disapproved based on these tests.
(iv) In-silico assays
Are biological experiments or tests conducted on a computer or a computer simulation. In-silico
uses virtual screening tools to make predictions about the behavior of different drug. It achieves
this by modelling the interactions between drugs and their targets.

3. There are several drugs that act that act in several pathways to eliminate such fungal infections.
The objective of the anti-fungal drug is to kill the fungal cell. Most of the fungal drugs do this by
altering the cell membrane permeability. However, there are drugs that kill the fungal cell by
blocking the nucleic acid synthesis and disrupting the microtubules. So, drugs that alters the cell
membrane permeability does it by inhibiting the synthesis of ergosterol or by binding to it. So
the synthesis of ergosterol starts from squalene. It is converted to 2,3-oxidosqualene by the help
of the enzyme known as squalene epoxidase, then it is converted to lanosterol. Lanosterol is
converted to ergosterol by the help of the enzyme called demethylase. In order to kill the fungal
cell, the drug needs to stop the synthesis of ergosterol. Terbinafine are a group of drugs that
inhibits this enzyme and stops the production of 2,3-oxidosqualene, so does inhibits the
production of ergosterol also. Azoles are the group of drugs that inhibits the demethylase enzyme
in order to inhibit the synthesis of ergosterol. Examples of azole drugs are fluconazole,
itraconazole, ketoconazole and miconazol. Not all drugs inhibit the synthesis of ergosterol. They
bind with ergosterol to show their effect. So there is a drug known as Amphotericin B that binds
with ergosterol in the fungal cell membrane and creates force in the cell membrane and from the
spores, the cell leaks out causing death of the fungal cell. There are some drugs which blocks the
synthesis of β-glucans which are present in the fungal cell wall by inhibiting the β-glucan
synthase enzyme which is present in the fungal cell membrane. The β-glucan synthase enzyme is
responsible for the production of β-glucans, so by inhibiting it can stop the production of
β-glucans, thus causing the alteration in the permeability of the fungal membrane and thus
causing the death of the fungal cell. Flucytosine are a group of drugs that kill the fungal cells by
blocking the synthesis of nucleic acids. Griseofulvin kills the fungal cells by disrupting the
microtubules of the fungal cell.
4.

5. Anti-viral drugs are medications used to treat infections. Anti-viral drugs do not kill viruses
but they inhibit viral reproduction by interfering with a certain stage of the virus life cycle. A
virus is composed of a genome, DNA or RNA, wrapped inside a protective protein coat, called a
capsid. Most animal viruses also have an additional lipid membrane, called an envelope, with
protein spikes that serve to attach to host cells. A viral life cycle typically consists of the
following steps: attachment to host cell receptor, followed by viral entry (via endocytosis,
membrane fusion, or both), release of viral genome (also known as un-coating), replication of
viral genome, synthesis and processing of viral proteins, assembly of viral components into new
viruses, and release of new viruses from host cell. Anti-viral strategies aim to block viral
reproduction at any of these stages. To prevent viral attachment, a drug can either bind to host
cell receptor/co-receptor, or to the viral spike protein. Examples are HIV drugs –
CCR5-antigonists. They bind to CCR5 co-receptor, masking its binding site for HIV. For
enveloped viruses, one strategy is to prevent fusion of viral and host cell membrane. An agent
can bind directly to the viral protein that is responsible for fusion, or disrupt the condition that is
required for fusion. Several drugs have been developed to inhibit the un-coating of influenza
virus, they impair the function of the protein responsible for viral genome release from
endosomes. Viruses that use reverse transcriptase for replication are usually targeted for this
enzyme. Because the process of reverse transcription converting RNA to DNA, occurs only in
these viruses not human cells, drugs targeting reverse transcriptase are generally safe for humans.
Most of these agents are nucleoside or nucleotide analogs. They compete with regular
nucleotides, insert themselves into the growing chain of DNA, and stop the process prematurely.
There are also non-nucleoside reverse transcriptase inhibitors, which bind non-competitively to
the reverse transcriptase, impairing its function. The two classes of inhibitors are usually
combined for maximum effects. Retroviruses, such as HIV, use viral enzyme integrase to insert
their genome into host cell DNA, a critical step for viral reproduction. Drugs that inhibit
integrase have been developed to treat HIV and other retroviruses. Viruses with large DNA
genomes usually encode their own DNA polymerase for DNA replication. Viral DNA
polymerases are the target of many currently available anti-viral drugs. Most of these drugs are
nucleoside analogs, they incorporate into the growing DNA and cause premature termination of
viral DNA synthesis. Another approach is to inhibit viral protein synthesis by antisense
mechanism. Antisense antiviral drugs are short synthetic nucleic strands that are complementary
to part of an essential viral mRNA. They bind specifically to the viral mRNA, effectively
preventing it from being translated into protein.

6.
a) Exposure to UV-radiation have many negative effects on skin, including erythema,
edema, sunburned cells, hyperplasia, inflammation, immunosuppression, photoaging, and
photocarcinogenesis. Treatment with flavonoids can minimize adverse skin reactions
caused by UV-radiation. The flavonoids protect the skin by absorbing the UV radiation
and blocking UV penetration.
b) Steroids modify the functions of epidermal and dermal cells and of leukocytes
participating in proliferative and inflammatory skin diseases. After passage through the
cell membrane, steroids react with receptor proteins in the cytoplasm to form a steroid
receptor complex. This complex moves into the nucleus, where it binds to DNA. The
binding process then changes the transcription of messenger RNA (mRNA). Because
mRNA acts as template for protein synthesis, steroids can either stimulate or inhibit the
synthesis of specific proteins. Thus corticosteroids are known to stimulate the production
of a glycoprotein called lipocortin. The formed lipocortin inhibits the activity of
phospholipase, which releases arachidonic acid, the precursor of prostanoids and
leukotrienes, from phospholipids. In contrast, corticosteroids inhibit mRNA responsible
for interleukin-1 formation. These actions of steroids on arachidonic acid metabolism and
interleukin-1 formation produce anti-inflammatory, immunosuppressive and
anti-mitogenic effects.