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Katherine Johnson’s mathematical calculations helped guide some of America’s most important early space missions while she confronted the racial and gender barriers faced by Black women in twentieth-century America.
MORE →Reflects the personal views, recollections, and perspective of the author, Mike Davis.
This is a personal recollection on the Move fire on May 13, 1985
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| Clinical data | |
|---|---|
| Other names | S-32504; S-32,504 |
| Routes of administration | Unspecified[1] |
| Drug class | Dopamine receptor agonist; Dopamine D2 and D3 receptor agonist |
| ATC code |
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| Identifiers | |
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| PubChem CID | |
| ChemSpider | |
| ChEMBL | |
| Chemical and physical data | |
| Formula | C16H22N2O2 |
| Molar mass | 274.364 g·mol−1 |
| 3D model (JSmol) | |
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S32504 is a dopamine D2 and D3 receptor agonist which was under development for the treatment of Parkinson's disease but was never marketed.[1][2][3] Its route of administration was unspecified.[1]
S32504 acts as a potent and selective agonist of the dopamine D3 and D2 receptors, with EC50 values of 2.0–3.2 nM and 2.5–398 nM, respectively, depending on the assay.[3] It is a preferential agonist of the dopamine D3 receptor over the dopamine D2 receptor.[3] The drug showed little affinity for or activity at more than 50 other receptors and targets, including the dopamine D1, D4, and D5 receptors and the serotonin 5-HT1A and 5-HT2A receptors, among others.[3] S32504 suppressed the activity of dopaminergic neurons in the ventral tegmental area (VTA) in rodents.[3] In addition, it potently reduced levels of dopamine in the striatum, nucleus accumbens, and frontal cortex, which could be reversed by the dopamine D2 and D3 receptor antagonist haloperidol and by the selective dopamine D2 receptor antagonist L-741,626, but not by the selective dopamine D3 receptor antagonist S33084.[3]
The drug produces antiparkinsonian effects in rodents and monkeys and antidepressant- and anxiolytic-like effects in rodents.[4][5] The antiparkinsonian effects of S32504 could be blocked by the dopamine D2 and D3 receptor antagonists haloperidol and raclopride and by L-741,626, but not by S33084, suggesting mediation of these actions by the dopamine D2 receptor and not by the dopamine D3 receptor.[4] However, the dopamine D3 receptor appeared to be involved in dopaminergic neuroprotective effects of S32504.[4] The antidepressant- and anxiolytic-like effects of S32504 were blocked by haloperidol, raclopride, and L-741,626 but not by S33084, again suggesting involvement of the dopamine D2 receptor and not the dopamine D3 receptor in these effects.[5] In rats treated with the dopamine depleting agent reserpine and monkeys treated with the dopaminergic neurotoxin MPTP, S32504 reversed hypolocomotion.[4] Conversely, in untreated rodents, S32504 produced hypolocomotion over a wide range of doses and did not produce hyperlocomotion at any assessed dose.[5]
Analogues of S32504 with enhanced affinity and selectivity for the dopamine D3 receptor over the dopamine D2 receptor have been developed and described.[6]
S32504 was first described in the scientific literature by 1999.[7][8]
S32504 was being developed for the treatment of Parkinson's disease by Servier in France.[1][2] It reached the preclinical research stage of development prior to its development being discontinued.[1][2] No recent development was reported by 2003.[1]
Source: Wikipedia. Article content is retrieved live through the MediaWiki API.
S32504 is a dopamine D2 and D3 receptor agonist which was under development for the treatment of Parkinson's disease but was never marketed. Its route of administration was unspecified.
Ketamine is a cyclohexanone-derived dissociative general anesthetic and NMDA receptor antagonist with analgesic and hallucinogenic properties, used medically for anesthesia, depression, and pain management. Ketamine exists as its two enantiomers, S- (esketamine) and R- (arketamine), and has antidepressant action likely involving NMDA antagonism as well as other mechanisms. At anesthetic doses, ketamine induces a state of dissociative anesthesia, a trance-like state providing pain relief, sedation, and amnesia. Its distinguishing features as an anesthetic are preserved breathing and airway reflexes, stimulated heart function with increased blood pressure, and moderate bronchodilation. As an anesthetic, it is used especially in trauma, emergency, and pediatric cases. At lower, sub-anesthetic doses, it is used as a treatment for pain and treatment-resistant depression. Ketamine is legally used in medicine but is also tightly controlled, as it is used as a recreational drug for its hallucinogenic and dissociative effects. When used recreationally, it is found both in crystalline, powder and liquid form, and is often referred to by users as "Ket", "Special K" or simply "K". The long-term effects of repeated use are largely unknown and are an area of active investigation. Liver and urinary toxicity have been reported among regular users of high doses of ketamine for recreational purposes. Ketamine can cause dissociation and nausea, and other adverse effects, and is contraindicated in severe heart or liver disease, and uncontrolled psychosis. Ketamine's clinical and antidepressant effects can be influenced by co-administration of other drugs, though these interactions are variable and not yet fully understood. Ketamine was first synthesized in 1962; it was derived from phencyclidine in pursuit of a safer anesthetic with fewer hallucinogenic effects. It was approved for use in the United States in 1970. It has been regularly used in veterinary medicine and was extensively used for surgical anesthesia in the Vietnam War. It later gained prominence for its rapid antidepressant effects discovered in 2000, marking a major breakthrough in depression treatment. Racemic ketamine, especially at higher doses, may be more effective and longer-lasting than esketamine in reducing depression severity. It is on the World Health Organization's List of Essential Medicines. It is available as a generic medication.
Lysergic acid diethylamide, commonly known as LSD (from German Lysergsäurediethylamid) and by the nicknames acid and Lucy, is a semisynthetic psychedelic drug derived from ergot, known for its potent psychological effects. LSD taken orally has an onset of action of 0.4 to 1.0 hours and a duration of 7 to 12 hours. In recreational settings it is commonly administered via tabs of blotter paper. LSD is extremely potent, with noticeable effects at doses as low as 20 micrograms and is sometimes taken in even smaller amounts for microdosing. Despite widespread use, no fatal human overdoses have been documented. LSD is mainly used recreationally or for spiritual purposes. LSD can cause mystical experiences. LSD exerts its effects primarily through high-affinity binding to several serotonin receptors, especially the serotonin 5-HT2A receptor, and to a lesser extent dopamine and adrenergic receptors. Neuroimaging studies indicate that LSD reduces the efficacy of thalamo-cortical information filtering (producing sensory overload), decreases oscillatory power within the default mode network, and flattens hierarchical organization of large-brain activity. At higher doses, it can induce visual and auditory hallucinations, ego dissolution, and anxiety. LSD use can cause hallucinogen-induced psychotic disorder where paranoia and delusions persist beyond the initial effects of the drug. LSD may lead to persistent visual disturbances known as hallucinogen persisting perception disorder (HPPD). Swiss chemist Albert Hofmann first synthesized LSD in 1938 and discovered its potent psychedelic effects in 1943 after accidental ingestion. It became widely studied in the 1950s and 1960s. The drug was initially explored for psychiatric use due to its structural similarity to serotonin and safety profile. It was used experimentally in psychiatry for treating alcoholism and schizophrenia. By the mid-1960s, LSD became central to the youth counterculture in places like San Francisco and London, influencing art, music, and social movements through events like Acid Tests and figures such as Timothy Leary, Owsley Stanley and Michael Hollingshead. Its psychedelic effects inspired distinct visual art styles and musical innovations, and caused a lasting cultural impact. However, its association with the counterculture movement of the 1960s led to its classification as a Schedule I drug in the United States in 1970. It was also listed as a Schedule I controlled substance by the United Nations in 1971 and remains without approved medical uses. Despite its legal restrictions, LSD remains influential in scientific and cultural contexts. Research on LSD declined due to cultural controversies by the 1960s, but has resurged since 2009. In 2024, the United States Food and Drug Administration designated LSD (code name MM120 or DT120) as a breakthrough therapy for generalized anxiety disorder. As of 2017, about 10% of people in the United States had used LSD at some point, with 0.7% having used it in the past year. Usage rates have risen, with a 56.4% increase in adult use in the United States from 2015 to 2018.
Modafinil, sold under the brand name Provigil among others, is a central nervous system (CNS) stimulant medication used to treat narcolepsy, sleep apnea, and shift work sleep disorder. It is taken by mouth. Modafinil is a first-line treatment for narcolepsy in the United States and Europe. The mechanism of action is not fully understood, but modafinil acts mainly as an atypical dopamine reuptake inhibitor, increasing dopamine levels without the rapid or overt signaling seen with classical stimulants such as amphetamine or cocaine. Unlike these drugs, modafinil has low addiction and dependence potential and does not produce strong euphoria, which contributes to its classification as a Schedule IV controlled substance in the United States. It is a prescription medication in most countries. Modafinil is generally well-tolerated; common side effects include headache, nausea, anxiety, and insomnia. Rare but serious adverse effects include severe skin reactions such as Stevens–Johnson syndrome. Modafinil is contraindicated during pregnancy due to increased risk of birth defects. Modafinil is used off-label as a cognitive enhancer by students and professionals seeking improved focus. Research on cognitive effects in non-sleep-deprived individuals has yielded mixed results. Modafinil is banned in competitive sports by the World Anti-Doping Agency. Modafinil was developed in France in the 1970s by neurophysiologist Michel Jouvet. The drug was approved for medical use in France in 1994 and in the United States in 1998. Generic versions became available in the US in 2012.
Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.
MORE →The Greenwood District.
