This is consistent with the observation that animal screening models indicate putative antidepressant activity for this compound, although one study has been negative. Formal clinical trials in depressed patients have not been reported.It has also been investigated for use in the treatment of cancer. Captopril stereoisomers were also reported to inhibit some metallo-β-lactamases. Adverse effects
Adverse effects of captopril include cough due to increase in the plasma levels of bradykinin, angioedema, agranulocytosis, proteinuria, hyperkalemia, taste alteration, teratogenicity, postural hypotension, acute renal failure, and leukopenia. Except for postural hypotension, which occurs due to the short and fast mode of action of captopril, most of the side effects mentioned are common for all ACE inhibitors. Among these, cough is the most common adverse effect. Hyperkalemia can occur, especially if used with other drugs which elevate potassium level in blood, such as potassium-sparing diuretics. Other side effects are:

Itching
Headache
Tachycardia
Chest pain
Palpitations
Dysgeusia
WeaknessThe adverse drug reaction (ADR) profile of captopril is similar to other ACE inhibitors, with cough being the most common ADR. However, captopril is also commonly associated with rash and taste disturbances (metallic or loss of taste), which are attributed to the unique thiol moiety. Overdose
ACE inhibitor overdose can be treated with naloxone. History
In the late 1960s, John Vane of the Royal College of Surgeons of England was working on mechanisms by which the body regulates blood pressure. He was joined by Sérgio Henrique Ferreira of Brazil, who had been studying the venom of a Brazilian pit viper, the jararaca (Bothrops jararaca), and brought a sample of the vipers venom.
Clinical diagnostic criteria were developed by Gordon et al. in 1967. They observed "persistent tonic contraction reflected in constant firing, even at rest" after providing patients with muscle relaxants and examining them with electromyography. In 1989, criteria for an SPS diagnosis were adopted that included episodic axial stiffness, progression of stiffness, lordosis, and triggered spasms. The name of the disease was shifted from "stiff-man syndrome" to the gender-neutral "stiff-person syndrome" in 1991.In 1988, Solimena et al. discovered that autoantibodies against GAD played a key role in SPS. Two years later, Solimena found the antibodies in 20 out of 33 patients examined. In the late 1980s, it was also demonstrated that the serum of SPS patients would bind to GABAergic neurons. In 2006, the role of GABARAP in SPS was discovered. The first case of paraneoplastic SPS was found in 1975. In 1993, antiamphiphysin was shown to play a role in paraneoplastic SPS, and seven years later antigephyrin was also found to be involved in the condition.In 1963, it was determined that diazepam helped alleviate symptoms of SPS. Corticosteroids were first used to treat the condition in 1988, and plasma exchange was first applied the following year. The first use of intravenous immunoglobulin to treat the condition came in 1994. See also
Satoyoshi syndrome
Hyperekplexia

References
Bibliography
Alexopoulos, Harry; Dalakas, Marinos (2010). "A Critical Update on the Immunopathogenesis of Stiff Person Syndrome". European Journal of Clinical Investigation. 40 (11): 1018–25. doi:10.1111/j.1365-2362.2010.02340.x. PMID 20636380. S2CID 30688501. Ali, Fatima; Rowley, Merrill; Jayakrishnan, Bindu; Teuber, Suzanne; Gershwin, Eric; Mackay, Ian (2011).