U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Status:
US Previously Marketed
Source:
piperocaine
(1933)
Source URL:
First marketed in 1933
Source:
piperocaine
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)



Piperocaine (Metycaine) is a local anesthetic drug. It is an ester and primarily is a sodium channel blocker. Piperocaine can partially inhibit dopamine. It is known as a alpha-1-proteinase inhibitor. Used in the form of its hydrochloride as a local or spinal anesthetic and in dental anesthesia. Can cause toxic reactions. Piperocaine Hydrochloride is in the list of Bulk Drug Substances Nominated for Use in Compounding Under Section 503A, FDA Act. Piperocaine hydrochloride is a small, white odorless crystals or a white crystalline powder, stable in air, freely soluble in water, alcohol and chloroform.
Status:
US Previously Marketed
Source:
Dinitrophenol
(1933)
Source URL:
First marketed in 1933

Class (Stereo):
CHEMICAL (ACHIRAL)


Conditions:

2,4-dinitrophenol (DNP) is a FDA-banned weight-loss agent and EPA-regulated environmental toxicant, traditionally used in research labs as an uncoupler of OXPHOS. Although not licensed for human consumption, DNP and DNP crystal form are used by bodybuilders and extreme dieters for their fat burning properties through inhibiting efficient energy (ATP) production in cells. Through uncoupling mitochondrial oxidative phosphorylation by facilitating proton transport across the mitochondrial membrane, DNP leads to rapid consumption of energy without generating ATP and consequently, to increased fat metabolism. However, the weight-loss effect comes with serious, and in some cases potentially fatal, adverse side effects, namely hyperthermia (the leading cause of fatality with acute DNP toxicity) and cardiac arrest, but also diaphoresis, tachycardia, tachypnea, skin toxicity, Fourier’s gangrene and cataracts with low dose chronic exposure. The proposed mechanism of DNP induced toxicity suggests the activation of ATP-sensitive K channels.
Status:
US Previously Marketed
Source:
hexobarbital
(1933)
Source URL:
First marketed in 1933
Source:
hexobarbital
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)


Conditions:

Hexobarbital or hexobarbitone, (sold both in acid and sodium salt, brand name Evipan, and Tobinal), is a barbiturate derivative having hypnotic and sedative effects. It was used in the 1940s and 1950s as an agent for inducing anesthesia for surgery, as well as a rapid-acting, short-lasting hypnotic for general use, and has a relatively fast onset of effects and short duration of action. It was also used to murder women prisoners at Ravensbruck Concentration Camp. Modern barbiturates (such as Thiopental) has largely supplanted the use of hexobarbital as an anesthetic, as they allow for better control of the depth of anesthesia. Hexobarbital is still used in some scientific research. Hexobarbital binds at a distinct binding site associated with a Cl- ionophore at the GABA-A receptor, increasing the duration of time for which the Cl- ionophore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.
Status:
US Previously Marketed
Source:
hexobarbital
(1933)
Source URL:
First marketed in 1933
Source:
hexobarbital
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)


Conditions:

Hexobarbital or hexobarbitone, (sold both in acid and sodium salt, brand name Evipan, and Tobinal), is a barbiturate derivative having hypnotic and sedative effects. It was used in the 1940s and 1950s as an agent for inducing anesthesia for surgery, as well as a rapid-acting, short-lasting hypnotic for general use, and has a relatively fast onset of effects and short duration of action. It was also used to murder women prisoners at Ravensbruck Concentration Camp. Modern barbiturates (such as Thiopental) has largely supplanted the use of hexobarbital as an anesthetic, as they allow for better control of the depth of anesthesia. Hexobarbital is still used in some scientific research. Hexobarbital binds at a distinct binding site associated with a Cl- ionophore at the GABA-A receptor, increasing the duration of time for which the Cl- ionophore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.
Status:
US Previously Marketed
Source:
piperocaine
(1933)
Source URL:
First marketed in 1933
Source:
piperocaine
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)



Piperocaine (Metycaine) is a local anesthetic drug. It is an ester and primarily is a sodium channel blocker. Piperocaine can partially inhibit dopamine. It is known as a alpha-1-proteinase inhibitor. Used in the form of its hydrochloride as a local or spinal anesthetic and in dental anesthesia. Can cause toxic reactions. Piperocaine Hydrochloride is in the list of Bulk Drug Substances Nominated for Use in Compounding Under Section 503A, FDA Act. Piperocaine hydrochloride is a small, white odorless crystals or a white crystalline powder, stable in air, freely soluble in water, alcohol and chloroform.
Status:
US Previously Marketed
Source:
Dinitrophenol
(1933)
Source URL:
First marketed in 1933

Class (Stereo):
CHEMICAL (ACHIRAL)


Conditions:

2,4-dinitrophenol (DNP) is a FDA-banned weight-loss agent and EPA-regulated environmental toxicant, traditionally used in research labs as an uncoupler of OXPHOS. Although not licensed for human consumption, DNP and DNP crystal form are used by bodybuilders and extreme dieters for their fat burning properties through inhibiting efficient energy (ATP) production in cells. Through uncoupling mitochondrial oxidative phosphorylation by facilitating proton transport across the mitochondrial membrane, DNP leads to rapid consumption of energy without generating ATP and consequently, to increased fat metabolism. However, the weight-loss effect comes with serious, and in some cases potentially fatal, adverse side effects, namely hyperthermia (the leading cause of fatality with acute DNP toxicity) and cardiac arrest, but also diaphoresis, tachycardia, tachypnea, skin toxicity, Fourier’s gangrene and cataracts with low dose chronic exposure. The proposed mechanism of DNP induced toxicity suggests the activation of ATP-sensitive K channels.