This document provides information about anti-tubercular drugs. It discusses various drugs used to treat tuberculosis (TB) including isoniazid, rifampicin, ethambutol, and pyrazinamide. It describes the mechanisms of action, side effects, dosages, and importance of combination therapy to prevent development of drug resistance in TB treatment.
2. ANTI-TUBERCULAR DRUGS
Tuberculosis (often called TB) is chronic bacterial infection caused by
“MYCOBACTERIUM TUBERCULOSIS, M. Bovos.
It contains unusual cell wall. The cell wall has a high lipid content,resulting
high degree of hydrophobicity and resistance to alcohol,acids, alkalies
and some disinfefectants.
This organism usually attacks or affects almost any tissue and lungs, but
can also affect the …
1. CNS (meningitis),Circulatory system,Genitourinary system,Bones,joints.
It is characterized by the formation of nodular bodies or tubercles( hence
the name tuberculosis)
• It is one of the most deadly and common major infectious disease
today, more than 2 billion people have been suffering the world’s
population.
1000 people have been dieing daily in India by TB.
TB spread person to person through the air.
When people with TB in their lungs or throat cough, laugh, sneeze, sing or
even talk the germs that cause TB may be spread into the air, if another
person breaths in these germs there is a chance that they will become
infected with TB.
(Anti mycobacterial drugs)
3. • Generally it spreads in crowded areas, elderly
persons AIDS patients, and severity of disease
Increased further in patients with
Diabetes mellitus
Hodgkin’s lymphoma
Chronic lung disease
Chronic renal failure
Malnutrition, and Immuno suppression.
Symptoms of TB:
• An unproductive cough.
• Feeling tired all the time.
• Weight loss, loss of appetite,Night time sweating.
• Fever, Coughing up blood.
• Fatigue, night sweats,constant tiredness.
• Chest x-ray examination reveals changes like pleural
effusion (increase volume of pleural space), diffuse infiltrates in
lung parenchyma. Untreated cases may show systemic
secondary amyloidosis ( infiltration of liver, kidneys, spleen and
other tissues with amyloid.
4. Chest X-Ray of Patient with Active
Pulmonary Tuberculosis
5. • Tuberculosis Treatment:
Because administration of a single drug
Often leads to the development of a bacterial
population resistant to the drug.
• Effective treatment of TB must contain
multiple drugs to which the organisms are
susceptible.
Definition:-
Anti-tubercular drugs are the agents which are
used to treatment of tuberculosis.
6. In 1938, Sulphanilamide was discovered and was found to possess bacteriostitac
Action although weak in nature.
Later Dapsone was developed, Although dapsone was effective it was not
Considered for clinical use because it demanded high doses which in turn
were associated with toxicity.
Eventually, many potent anti-tubercular drugs were developed in to order
Streptomycin
PASA
Isoniazid
Ethambutol
Rifampicin etc.
The discovery of Rifampicin was a major break through in the treatment of
Tuberculosis.
This is because combination of Isoniazid, ethambutol and Rifampicin required
Comparatively less time for producing effective results than the individual drugs
Used alone.
Since then combination of the three drugs have acquired prime importance in
The treatment of tuberculosis.
7. First- line drugs are those which exhibit high efficacy and less toxicity
All first-line anti-tuberculous '''drug names'''
have a standard three-letter and a single-letter abbreviation:
* [[Ethambutol]] is EMB or E,
* [[isoniazid]] is INH or H,
* [[pyrazinamide]] is PZA or Z,
* [[rifampicin]] is RMP or R,
* [[streptomycin]] is STM or S.
Second line drugs:
Second-line drugs for tuberculosis are found to be more toxic but may
required with certain resistance problems
There are six classes of second-line drugs (SLDs) used for the treatment of TB. A
drug may be classed as second-line instead of first-line for one of three possible
reasons: it may be less effective than the first-line drugs (e.g., p-aminosalicylic acid);
or, it may have toxic side-effects (e.g., cycloserine); or it may be unavailable in many
developing countries (e.g., fluoroquinolones):
Aminoglycosides: Amikacin(AMK) Kanamycin(KM)
Fluroquinolones: Ciprofloxacin(CIP), Levofloxacin.
Thioamines: thionamide.
P-amino salicylic acid(PAS)
Polypeptides: Viomycin, Enviomycin, Capreomyhcin.
Cycloserine(The only antibiotic in its class)
Classification :
Anti-tubercular drugs are classified on the basis of efficacy and safety clinical utility
8. • Third line
• Other drugs that may be useful, but are not on the WHO list .These
drugs may be considered "third-line drugs" and are listed here either
because they are not very effective (e.g., clarithromycin) or because
their efficacy has not been proven (e.g., linezolid, R207910).
Rifabutin is effective, but is not included on the WHO list because
for most developing countries, it is impractically expensive.
9. Antitubercular drugs are also classified on the basis of
Chemical moiety as:-
1.Salicylic acid derivatives:
Para amino salicylic acid.
2.Pyridine derivatives:
Isoniazid (Isonicotinic acid hydrazine) ,Ethionamide, Prothionamide.
3.Pyrazine derivatives:
Pyrazinamide
4.Ethylenediaminobutanol derivatives:
Ethambutol.
5.Antibiotics:
Streptomycin, Refampin (Refampicin), Kanamcin.
6.Miscellaneous drugs:
Fluoroquinolones: Ofloxacin ,Ciprofloxacin.
Macrolides: Clarithromycin,,Azithromycin.
10. ISONICOTINIC ACID HYDRAZINE( ISONIAZID),INH:
Isonicotinic acid hydrazine (INH) first synthesized in 1952.
It is a first-line synthetic anti-tubercular drug having bacteriostatic action.
It is also known as isoniazid,INH,Isonicotinohydrazine(Nydrazid,Lanizid)
Although it is effective when used alone, combination of it with other drugs
Refampicin is preferred firstly, to avoid the development of resistance to words
the drug by tubercle bacilli and to achieve good therapeutic effects and also
Avoid high doses of isoniazid.
Structure:
It is a very simple derivative of pyridine, and also one of the cheapest
Anti-tubercular drug.
Pyridine-4-corboxylic acid hydrazide.
11. Mechanism of action/mode of action:-
Exact mechanism of action of isoniazid is not known; although several mechanisms
Have been reported.
The mechanism of action might involve the displacement of nicotinamide by isoniazid
In an enzyme.
Basically Isoniazid is a prodrug and is activated by oxidation to isonicotinaldehyde,
Isonicotinic acid, iso nicotinamide.
The enzymecomplex catalase peroxide responsible for oxidation which is found in bacilli.
.(present in mycobacterium)
This inactive enzyme-drug complex try to change the metabolism of proteins,
Nuclic acids, lipids and carbohydrates.
INH is highly selective towards Mycobactera. These bacterial cell walls are made up of
Mycolic acids. Mycolic acids is an important constituents of mycobacterial cell wall
If Mycolic acid synthesis inhibited, causing in loss of some areas of outer
membrane and thinness of the cell wall.
Isoniazid(INH) Isonicotinaldehyde Isonicotinic acid Isonicotinamide
catalyzed by an endogenous
enzyme KatG
12. • Isoniazid specifically inhibits long-chain fatty acid synthesis
(>26 carbon atoms) lipids having a short arm of 20-24 carbon
atoms and a long arm of 50-60 carbons. It has been proposed
thatINH is activated to an electrophilic species that acylates the
four position of the NADH.The acylation of unsaturated fatty
acids which are essential for the synthesis of the mycolic acids.
13. SAR OF ISONIAZID:
a. The N-1 nitrogen in hydrazine side chain should be unsubstituted.
b. N-2 Nitrogen can be substituted with alkyl groups to get active compounds.
c. Replacement of pyridine nucleus with other aromatic ring such as
benzine or piperidine or thiazole ring diminished the anti-tubertcular activity.
d. Neumerous derivatives have been developed none of them have
exhibited activity superior to that of the parent drug.
e. When isopropyl group is substituted at R2, the resultant was a N2
isopropyl derivative named iproniazid. This drug apart from
antitubercular activity it was also found to exhibit psychomotor stimulant
activity.
N
O OH
isonicotinic acid
OHN
NH2
N
isoniazid
N
CH3
4-methyl pyridine
Oxidation H2NNH2
Anhydrous
hydrazine
Synthesis of isoniazid:
14. • Metabolism of Isoniazid:
• Isoniazid is metabolized in the liver via acetylation. There are two forms of
the enzyme responsible for acetylation, so that some patients metabolize
the drug more quickly than others. Hence, the half-life is bimodal with peaks
at 1 hour and 3 hours in the US population. The metabolites are excreted in
the urine. Doses do not usually have to be adjusted in case of renal failure.
Metabolism of isoniazid
15. Physico-chemical properties:
soniazid is a colorless, odourless,sweet to bitter, crystalline, easily soluble in
Alcohol, water and partially insoluble in ether and benzene.
Adverse effects:
The most common side effects is peripheral neuritis, optic neuritis,hepatotoxicity,
Anorexia,weakness,fever,fatigue,Nephrotocicity,prupra,urticaria,anaemia,eosinophilia
Coagulation,granulocytosis,nausea,vomiting,restlessness and dryness of mouth.
Toxic doses may cause hyperglycemia,glycosuria,seizures and even coma.
Therapeutic uses:
1. Treatment of tuberculosis. Usually 2 or 3 agents together or alone for prophylaxis
of TB.
2.Pridoxine (Vit-B6) is given together with the isoniazid to correct the
oxic reactions of INH.
3.It is first line drug. It is generally used with the other anti-tubercular drugs in
multiple drug theoay to lower the doses of other active drug and achieve effectiveness.
Adult dose: Each tablet contains:
Isoniazid--------50mg.
Rifampicin-----120mg.
Pyrazinamide—300mg.
This dose is to be taken on empty stomach. One hour prior or 2 hours after meals. for
2 months
Continuation phase: Isoniazid and rifampicin are to be used for next 4-months
(2 times/week.
4.It is used in the treatment of latent TB.
16. • Treatment of tuberculosis
• Single drug therapy is resistance to TB,that's why 4 drug
regimens are given genarally
• Then treatment is started with
• INH and
• Refanpin
.
Pyrizinamide and Ethambutal also given.
These two drugs should stop after 2 months and another
4 months INH and Rifampin should be given.
6-months
Mycobacteria are very-slow-growing organisms that grow both intracellularly
and extracellularly. Because of their growth,the treatment of mycobacterial
infections,especially tuberculosis,requires long-term treatment with a combination
of agents to effectively eradicate the disease and prevent resistance.
17. ETHAMBUTOL(Myambutol)
• Ethambutol abbreviated as EMB.
• The dextro enantiomer (+) is almost 200-500 times more potent than the
meso(-) -enantiomer.
• Levo isomer is pharmacologically inert.
• Structurally it possesses aliphatic diamine and two butanol moieties.
• Ethambutol is a water-soluble,bacteriostatic agent that is readily absorbed
(75-80%) following oral administration.
(Ethylenediaminobutanol derivatives)
2,2’-(1,2-ethanediyldiamino)bis-1-butanol.
18. SAR:1. The presence of two amino moieties is essential for antimicrobial activity.
Presence of small branched alkyl groups on the nitrogen atom also influences
the activity
2. When amino moieties were replaced by either acetyl,sulphonyl or nitrosyl
moieties antimycobacterial activity was abolished.
3.When heteroatoms such as oxygen, sulphur group were substituted in
ethylene moiety , inactive derivatives were obtained.
4.when hydroxyl groups were replaced with -0CH3or 0C2H5 equipotent
activity as that of parent drug–OH groups .
5 Replacement of by benzoyl,thiomethyl –NH2NHR results in
inactive compounds.
Ethambutol is bacteriostatic against actively growing TB bacilli. It works by
obstructing the formation of cell wall. Mycolic acids attach to the 5'-hydroxyl
groups of D-arabinose residues of arabinogalactan and form mycolyl-
arabinogalactan-peptidoglycan complex in the cell wall. It disrupts
arabinogalactan synthesis by inhibiting the enzyme arabinosyl transferase.
Disruption of the arabinogalactan synthesis inhibits the formation of this
complex and leads to increased permeability of the cell wall
Mechanism of action:
19. • Metabolism of ethambutol:
The majority of the administered EMB is excreted nchanged (73%),with
no more than 15% appearing in the urine as either motabolite A or
Metabolite B.
Both metabolites are devoid of biological activity.
20. Synthesis:
Physicochemical properties:
It is odorless, bitter,M.P=199-204o
C., Freely soluble in the water and alcohol and
Slightly soluble in chloroform.
Adverse/toxic effects:-
Optic neuritis resulting in decreased vision and loss of ability to differentiate red,
Green colours.
Nausea,anorexia,rashes,fever and hyperuricaemia.
Therapeutic uses:
It is first line drug used in the treatment of Pulmonary and extrapulmonary TB.
It is use in the prophylactic treatment of TB at dose if 15mg/kg/day
In the combination therapy of TB it is given along with Isoniazid,Pyrazinamide,
Rifampicin for 48 days(initial phase therapy).
It is prepared by first resolving resimic 2-aminobutanol via its tartrate and the (+)-
Enantiomorph is condensed with 1,2- dichloroethane in a in a suitable dehydro-
Chlorinating atmosphere, the resulting atmosphere is dissolved in appropriate
Solvent and treated with Hcl to obtain the official compound.
21. Rifampicin (Rifampin)
•Refamycins are a group of macrocyclic antibiotics which are
Produced by Streptomyces mediterranei.
Refamycins inhibit the enzyme RNA polymerase and prevent
RNA synthesis.Than in turn prevent protein synthesis.
•So they are useful in treating tuberculosis, leprosy,
Mycobacterium avium complex (MAC) infection, and
Staphylococcus infections.
•Eventually 7, rifamycins were developed they are
Rifamycin A,B,C,D,E,S,SV.
•Refampicin is a semi-synthetic rifamycin made from
Rifamycin-B isolated from streptomyces mediterranei in 1957
•Among the various rifamycins, rifamycin-B was the first
Commercial product.
22. Mechanism/mode of action:
Refampin is bactericidal at 0.005-0.2micrograms/ml vs
Micobacterium tuberculosis.
Rifampicin inhibits Grampositive bacteria and works by
Binding non-covalently to DNA-dependent RNA polymerase
and inhibiting the start of RNA synthesis
The DNA-dependent RNA polymerases in eukaryotic cells
are unaffected, since the drug binds to a peptide chain not
Present in the mamalian RNA polymerase. Therefore it is
highlyselective..
It acts by inhibiting DNA-dependent RNA polymerase
(DDRP)of mycobacteria and other microorganisms
by binding strongly to their β-subunits viz ( α, α1
, β, β1
And sigma) and there by supression of inhibiting the m-RNA synthesis
23. •Intact macrocyclic molecule is required for antimycobacterial activity.
•Double bonds in macrocyclic ring should not be redcuced ,or opening of the macro ring
results in compounds have decreased activity.
• Free hydroxyl groups should be present at c-1,c-8,c-21,c-23 all lie in a plane and play a
role in acting as binding groups for attachment to DDRP.
• When –OH groups at c-21 and c-23 were completely removed or substituted the
formation of derivatives are devoid of anti-mycrobial activity were obtained.
•Activity of the compounds get diminished when the –OH groups at c21 and c23 are
acetylated.
• The maintenance of drug activity relies on the presence of either –OH or carbonyl
group
both of which should be unsubstituted.
•Refampicin compound is formed by substitution of [(4-methyl-1piperazinyl)imino)methyl]
rd
Flat naphthalene ring and
Several of the –OH groups
Are essential for activity.
It is a zwitterion, and has good
Solubility both lipids and aqueous acid.
24. Uses:-
1.Refampicin is used as a first line drug in the treatment of tuberculosis. As most of the
tubercle bacilli develop resistance to rifampicin. It is used in combination with other
anti-tubercular drugs in the multiple drug therapy to minimize the problum.
It is also used the treatment of leprosy.
For prophylaxis in people exposed to meningococcemia or H. influenzae type
B meningitis.
Adult dose: Each tablet contains
Genarally the following dosage regimen is given
Rifampicin----120mg.
Isoniazid ------50mg.
Pyrimethamine-300mg.
4 tablets/day for patients ≤ 44kg.
6 tablets /day for patients ≥ 55kg.
child dose:- 100mg/kg of body weight as a single dose.
Continuation phase:-
Two drugs i.e. Rifampicin and isoniazid are to be used for a time period of the next
4months. (2 times/week)
Isoniazid---15mg/kg(orally),Rifampicin—10mg/kg (upto60mg/dose).
It is used in the first-line therapy of brucellosis in combination with doxycline.
25. • The drug is bactericidal and is mainly used in the treatment of
tuberculosis and staphylococci infections.
• It is also used in combination with dapsone in Treating leprosy.
• It is a very useful antibiotic, showing a high degre of selectivity
against bacterial cells over mammalian cells.
Unfortunately, it is so expensive, which discourages its use against
a wide range of infections.
26. Anti-leprotic drugs
• The drugs which are used in the treatment of leprosy are termed
antileprotic drugs.
• Leprosy is an infectious disease caused by a bacillus,
Mycobacterium leprae.
M. Leprae multiplies very slowly the incubation period for the
disease is about 5 years.
• Leprosy is not highly infectious. It is transmitted via droplets, from
the nose and mouth during close and frequent contact with those
infected who are not on treatment of multi drug therapy.
• Leprosy mainly affects the skin and peripheral nerves.
Signs of leprosy:-
A leprosy patient is someone who has a skin patch or patches with a
definite loss of sensation and who has not completed a full course of
treatment with Multidrug therapy.
Leprosy patches:-
• Can be pale or reddish or copper-colored
• Can be flat or raised
• Donot itch,usually don’t hurt, lack sensations to heat, touch or pain
• Can appear anywhere.
27. Discovered by Gerhard
Armauer Hansen in 1873
Global Project on the History of Leprosy
http://www.leprosyhistory.org/graphics/gallery/hansen.jpg
The bacteria that causes Leprosy, (mycrobacterium
Leprae) was discovered by Gerhard Hansen in 1873
Leprosy was known since ancient times, but no
one knew what it was or what caused it.
Armadillo
Some types of
monkeys Rabits Mices
Transmission
Nasal/oral Droplets
Dermal Inoculations
28. • Diagnosis of leprosy:-
Leprosy can be easily diagnosed on clinical signs
alone. The main diagnostic sign is loss of feeling in
the affected skin and unique to the disease. The
diagnosis can be made by gently touching the
affected areas with a pointed object like a pen.
Comparison can then be made with the sensation in
normal skin.
In earlier times, chaulmoogra oil was found to be
effective in the treatment of leprosy.
Next this herbal remedy was replaced by sulphones.
The prototype drug of these sulphones is dapsone
which is still using as an antileprotic drug.
Other drugs which find their use in the treatment of
leprosy are Clofazimine, certain tuberculars
(rifampicin, ethionamide) and antibiotics.
29. How the Human Body is
Affected by leprosy
Nerve is
damaged and
broken by
leprosy
infection.
Large bumps (legions)
on the skin that do not
heel and cannot feel
pain.
Nerve
Leprosy infection
30. classification:
• 1.Sulfones: Dapsone,solapsone,Acedapsone.
• 2.Phenazines: Clofazimine.
• 3.Thiosemi carbazones: Amithiazone.
• 4.Antitubercular drugs: Rifampicin,Ethionamide.
• Antibiotics:Ofloxacin,Clarithromycin,Minocycline.
• Natural oils: Chaulmoogra oil,Hydnocarpus oil.
Drug for the treatment of leprosy:
Sulfones: Most widely used sulphone is Dapsone.
Sulphones were fist used in the treatment of leprosy
In 1941.
4,4'-Diaminodiphenylsulfone(Dapsone)
31. Mechanism of action of Dapsone
• Dapsone acts by the same mechanism of action as that of sulfonamides. i.e.
completely antagonizing PABA.(inhibited by PABA incorporation in to folic
acid).
It acts by inhibiting the enzyme dihydropteroate synthase or folic acid synthetase
during the bacterial synthesis of tetrahydrofolic acid.
Inhibition of tetrahydrofolic acid production leads to decreased levels of purines
and nucleic acid which is necessary for the synthesis of proteins by the
bacteria.
Hence dapsone exerts a bacteriostatic action on M.leprae and acts as antileprotic.
Moreover dapsone exhibits the same antibacterial activity as that of
sulfonamides.
Both dapsone and clofazimine have significant anti-inflammatory actions
Metabolism of Dapsone:
The major metabolic product of
dapsone results from N-acetylation
in liver by N-acetyl transferase.
It also undergoes N-hydroxylation
to hydroxylamine derivate.
These metabolic reactions are
catalyzed by CYP3A4 isoforms.
Neither of these compounds
possesses leprostatic activity.
32. When benzene rings of dapsone was
replaced with thiazole ring
Thiazolsulfone was obtained which is
less activity when compared with
DDS( Dapsone)
When the phenyl rings(aromatic ring) of
dapsone were substituted with suitable
groups the derivatives possessed less
activity than the parent drug. Exception:
Aceto sulfone
Acedapsone, a prodrug of
dapsone. R= -COCH3. This
derivative is used as a depot
inj. Which is released very
slowly than parent drug.
acetosulfone reduced activity
while increasing water
solubility and decreasing
GI irritation.
•Infact none of the obtained derivatives
proved to be superior than dapsone.
Substitution of –CH2SO2Na
(methanesulfinate)
for R gave sulfoxone
Sodium forms Solapsone
(a prodrug of dapsone).
The amount required for
sulfoxone is thrice that of
dapsone.This can give
patients who are unable to
tolerate dapsone induced
GIT irritation.
.
SAR OF DAPSONE:
34. Physico chemical properties
• It is a white or creamy white,odourless,slightly bitter crystalline,
sparingly soluble in alcohol, slightly soluble in water.
Adverse/toxic effects:
Same adverse effects as those exhibited by sulfonamides.
Nausea,vomiting anoroxia,Dermatitis,drug fever ,Hepatitis,psychosis.
USES:-
1. Dapsone is used for the treatment of Multibacillary leprosy.
Dapsone100mg+Clofazimine-50mg for 12 months.
2. Paucibacillary leprosy:100mg/day for 6months.
3. Dermatitis herpetiformis (itching, lesions (similar tourticaria)
4. Treatment of pneumonia in AIDS. In this case co-administred
with trimethoprim.
5 Together with pyrimethamine + dapsone is used as
prophylactic measure against malaria.
6. Treatment of inflammatory disorders, polychondritis and
leishmaniasis.
35. Clofazimine(Lamprene):
It is classified as a secondary drug for the treatment of leprosy and commonly
used as a component of multidrug therapy.
The chemical, a phenazine derivative,is a water-insoluble
dye(dark-red crystals) that leads to pigmentation of the skin.
In addition,discoloration (pink,red or brownish-black)of the feces,eyelid
lininig,sputum,sweat,tears and urine is seen.
Mechanism of action:
The mechanism of action remains unclear at the present time.
It has been shown that clofazimine increases prostaglandin synthesis and the
generation of antimicrobial reactive oxidants from neutrophils,which may play
a role in the antileprosy effects.
The host cell defense may be stimulated by clofazimine,resulting in the generation
of oxidants,such as the super oxide anion,which in turn could have a lethal effect
on the organism.
36. • SAR of CLOFAZIMINE:
substituents on the imino group
at position 2 is essential.
imino group is substituted with
alkyl and cycloalkyl groups
activity is increased.
Halogensubstitution on para position of the
2 phenyls at C-3 and N-10 enhance activity.
The following order of activity has been
reported Br>Cl>CH3>Eto>H or F.
2
1
3
10
7
The chemical phenazine
nucleus is essential for
antimycobacterial and immuno-
suppressive properties.
Clofazimine was first used
to treat advanced leprosy
unresponsive to dapsone
or STM in 1966.
37. • Metabolism of clofazimine:
• Various metabolites of clofazimine have been identified but these account
for these account for less than 1% of the administered dose.
• The elimination of the clofazimine from the body is very slow(estimated
half life of from 8.8 to 69 days).
• The liphophilic nature of clofazimine results in distribution and storage of
drug in fat tissue.
• clofazimine undergo hydroxylic dehalogenation on the 3-chloroaniline
followed by sulfate conjugation and 4-hydroxylation followed by glucuronic
acid conjugation.
Human metabolic products of
Clofazimine.
38.
39. • Side effects:
The medication treats a common form of leprosy known as lepromatous leprosy,
and it works best when used in conjunction with another leprosy drug such as
dapsone. Clofazimine produces few serious side effects in most patients, but
the medication's gastrointestinal effects can become life-threatening.
Taking clofazimine frequently changes patients' skin color, making it redder or
browner.
• Other common side effects patients have reported include dry and flaky skin,
itching skin, rash, eye irritation, darkening of the whites of the eyes, high
blood sugar and darkening of the body's excretions (urine, sweat, feces).
Uses of clofazimine:
• clofazimine – an antibiotic drug that was originally designed to treat TB but
didn’t work, and is now used to treat leprosy – could bring benefits to people
with multiple sclerosis and other immune diseases, such as psoriasis and type
1 diabetes.
• Because clofazimine has already been used to treat leprosy, and is
relatively safe, it’s likely that it will be fast-tracked into clinical trials for
autoimmune diseases in the future.