{"id":3898,"date":"2022-10-03T12:54:40","date_gmt":"2022-10-03T12:54:40","guid":{"rendered":"https:\/\/modafinil.pl\/?post_type=product&p=3898"},"modified":"2026-10-03T05:28:11","modified_gmt":"2026-10-03T05:28:11","slug":"coluracetam","status":"publish","type":"product","link":"https:\/\/modafinil.pl\/en\/sklep\/coluracetam\/","title":{"rendered":"Coluracetam (CAS 135463-81-9) \u2014 Chemical Reagent 1000 mg, Purity \u2265 99%"},"content":{"rendered":"

N-(2,3-dimethyl-5,6,7,8-tetrahydrofuro[2,3-b]quinolin-4-yl)-2-(2-oxopyrrolidin-1-yl)acetamide<\/strong>, crystalline powder, 1000 mg package. Material intended exclusively for laboratory and analytical in vitro research<\/strong>. The product is not intended for consumption by humans or animals<\/strong>, it is not a medicinal product, a dietary supplement, a foodstuff, or a cosmetic.<\/p>\n

A thing that needs to be said up front<\/h2>\n

The literature on this molecule has an unusual shape worth knowing before reading further. Coluracetam is a compound chemically well-defined and with a real, though narrow, body of preclinical research<\/strong> \u2014 the problem is that most of it is indexed in databases not under the current common name, but under the development code from the period of laboratory work, MKC-231<\/strong>. A PubMed query for just the term “coluracetam” returns in practice a single record; only extending the query with the development code reveals the proper set of papers.<\/p>\n

The second caveat is more important: this entire body of work consists of mechanistic and behavioral studies in laboratory animals<\/strong>, conducted mainly between 1994 and 2008. None of it includes a published clinical study involving humans. The ChEMBL database classifies the compound’s development status as preclinical<\/strong> (development phase: 0) \u2014 meaning the compound formally never entered a documented clinical research program as understood by that database. The description below sticks to what can be reliably supported: chemistry, the cellular mechanism studied in animals, and registry data. We do not attribute any effect in humans to this molecule in the present tense \u2014 we have no source basis for that.<\/p>\n

Three different entities that must not be confused<\/h2>\n\n\n\n\n\n\n\n
Separating the layers: substance \u2014 medicinal product \u2014 reagent<\/caption>\n
Entity<\/th>\nWhat it is<\/th>\nStatus of coluracetam<\/th>\n<\/tr>\n<\/thead>\n
Chemical substance
CAS 135463-81-9<\/th>\n		A chemical concept \u2014 a molecule with a defined structure, registered in registry databases (PubChem, ChEMBL).<\/td>\nyes<\/strong> \u2014 this is the only status this molecule actually has<\/td>\n<\/tr>\n
Medicinal product<\/th>\nPharmaceutical preparation: pharmaceutical form, GMP regime, registration documentation, safety oversight.<\/td>\nNO \u2014 in any country.<\/strong> The compound was the subject of development work under the code MKC-231, but it never achieved registration as a drug; ChEMBL records its status as preclinical<\/td>\n<\/tr>\n
Chemical reagent
the material offered here<\/th>\n		Material for laboratory and analytical work.<\/td>\nyes<\/strong> \u2014 and it is offered exclusively in this capacity<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

The situation is closer to flmodafinil than to modafinil: there is no registered drug here from which the reagent would need to be distinguished<\/strong> \u2014 no approved form of this substance intended for humans exists in any jurisdiction. The research results cited below come exclusively from experiments in laboratory animals<\/strong> \u2014 none of them were conducted using the analytical reagent, and none of them transfer to the material offered here.<\/p>\n

Reagent identification card<\/h2>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
Registry data and identifiers \u2014 coluracetam<\/caption>\n
Systematic name (IUPAC)<\/th>\nN-(2,3-dimethyl-5,6,7,8-tetrahydrofuro[2,3-b]quinolin-4-yl)-2-(2-oxopyrrolidin-1-yl)acetamide<\/td>\n<\/tr>\n
Common name<\/th>\ncoluracetam (coluracetamum)<\/td>\n<\/tr>\n
Development codes<\/th>\nMKC-231, BCI-540<\/td>\n<\/tr>\n
CAS number<\/th>\n135463-81-9<\/td>\n<\/tr>\n
Molecular formula<\/th>\nC19<\/sub>H23<\/sub>N3<\/sub>O3<\/sub><\/td>\n<\/tr>\n
Molar mass<\/th>\n341.4 g\u00b7mol\u22121<\/sup><\/td>\n<\/tr>\n
Monoisotopic mass<\/th>\n341.17394 Da<\/td>\n<\/tr>\n
InChIKey<\/th>\nPSPGQHXMUKWNDI-UHFFFAOYSA-N<\/td>\n<\/tr>\n
SMILES<\/th>\nCC1=C(OC2=NC3=C(CCCC3)C(=C12)NC(=O)CN4CCCC4=O)C<\/td>\n<\/tr>\n
PubChem CID<\/th>\n214346<\/a><\/td>\n<\/tr>\n
ChEMBL ID<\/th>\nCHEMBL535678<\/td>\n<\/tr>\n
Form<\/th>\ncrystalline powder, white to off-white<\/td>\n<\/tr>\n
Purity<\/th>\n\u2265 99%<\/td>\n<\/tr>\n
Intended use<\/th>\nresearch reagent \u2014 not for consumption by humans or animals<\/strong><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Origin of the molecule: a Japanese “choline uptake enhancer”<\/h2>\n

Coluracetam did not arise as a derivative of piracetam in the sense of a strict modification of an existing drug. It is a separate research line developed in Japan, where the starting point was not the structure of a specific compound but function<\/strong>: a molecule was sought that would enhance high-affinity choline uptake (HACU, high-affinity choline uptake<\/em>) \u2014 the rate-limiting step in acetylcholine synthesis in cholinergic neurons. The compound received the development code MKC-231<\/strong>, under which the entire early literature from 1994\u20132008 is listed. The current common name “coluracetam” and the second development code, BCI-540<\/strong>, appear only in later chemical registries (ChEMBL) \u2014 earlier papers do not use them, which is itself a bibliographic clue, not just a curiosity.<\/p>\n

The cholinergic lesion model as the axis of research<\/h3>\n

The first indexed papers date from the mid-1990s and describe the compound’s behavior in a working memory deficit model induced by ethylcholine aziridinium ion (AF64A) in rodents \u2014 a standard pharmacological method for mimicking the cholinergic loss seen in dementias. In subsequent years, the same model was used to systematically describe the mechanism: effects on acetylcholine synthesis and release, long-term improvement in memory test results after repeated administration and \u2014 separately \u2014 the molecular mechanism of choline uptake enhancement itself. Three papers on this topic appeared together in 2008 in the Journal of Neural Transmission<\/em> and constitute the most systematic set of mechanistic data on this molecule that exists.<\/p>\n

The cytoprotective thread and the schizophrenia model<\/h3>\n

In parallel, cytoprotective studies were conducted in cortical neuron cultures (protection against glutamate cytotoxicity), along with studies on the compound’s effect on carbohydrate metabolism in animals. A separate branch of the literature concerns a pharmacological model resembling schizophrenia: administration of phencyclidine (PCP) to rodents causes loss of septal cholinergic neurons and behavioral deficits, and prior exposure to the compound antagonized part of these changes in an animal study. This is a study in an animal model, not a clinical observation<\/strong> \u2014 we cite it as part of the history of mechanistic research, not as evidence of effects in humans.<\/p>\n

Separately, in a review paper on the pharmacology of compounds modulating glutamatergic transmission in the context of the search for new antidepressant drugs, coluracetam was listed alongside ketamine, riluzole, memantine, and several experimental compounds as one of the candidates considered in this area [1<\/a>]. This is a mention in a review paper, not a standalone clinical study \u2014 we flag it because it is the only place where the molecule appears in literature indexed under its current common name, rather than under the code MKC-231.<\/p>\n

Timeline<\/h2>\n\n\n\n\n\n\n\n\n
Timeline: mechanistic research on the molecule (data verified in PubMed)<\/caption>\n
1994<\/th>\nfirst indexed papers on the compound under the code MKC-231 \u2014 AF64A working memory deficit model in rodents<\/td>\n<\/tr>\n
1998<\/th>\ncytoprotective studies: protection against glutamate cytotoxicity in cortical neuron culture<\/td>\n<\/tr>\n
1999<\/th>\nstudies on the compound’s central effect on carbohydrate metabolism in rats<\/td>\n<\/tr>\n
2007<\/th>\nstudy in a pharmacological model resembling schizophrenia \u2014 antagonizing phencyclidine (PCP)-induced deficits in animals<\/td>\n<\/tr>\n
2008<\/th>\nthree-part series of papers in Journal of Neural Transmission<\/em>: mechanism, acetylcholine synthesis\/release, cognitive effects after repeated administration in the AF64A model<\/td>\n<\/tr>\n
2015<\/th>\ncompound listed in a review of the pharmacology of glutamatergic antidepressant candidates [1<\/a>]<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Chemistry: the pyrrolidinone core and the furoquinoline system<\/h2>\n

Why the structure is classified in the racetam family<\/h3>\n

The molecule contains a 2-oxopyrrolidine<\/strong> ring (\u03b3-butyrolactam) connected by an acetamide group to the rest of the skeleton \u2014 exactly the same pharmacophoric motif that defines the entire racetam family, starting with piracetam. It is this that qualifies coluracetam for this structural category, not resemblance to any specific other molecule from this family.<\/p>\n

What the furoquinoline system adds<\/h3>\n

The second part of the molecule distinguishes it from simpler racetams: instead of a single aromatic ring (as in aniracetam), coluracetam carries a fused tricyclic system<\/strong> \u2014 a furan fused to a quinoline ring, partially hydrogenated at positions 5,6,7,8, and substituted with two methyl groups at positions 2 and 3. Three nitrogen atoms in the molecule (pyrrolidinone, quinoline, amide) and three oxygen atoms give the molecular formula C19<\/sub>H23<\/sub>N3<\/sub>O3<\/sub> \u2014 significantly larger and more complex than in piracetam or aniracetam.<\/p>\n\n\n\n\n\n\n\n\n\n\n
Computed descriptors and their analytical significance<\/caption>\n
Parameter<\/th>\nValue<\/th>\nWhat this implies<\/th>\n<\/tr>\n<\/thead>\n
Partition coefficient (XLogP)<\/th>\n2.4<\/td>\nmoderate lipophilicity \u2014 elutes later in an RP-HPLC gradient than simple racetams<\/td>\n<\/tr>\n
Topological polar surface area (TPSA)<\/th>\n75.4 \u00c52<\/sup><\/td>\nsimilar to modafinil (79.4 \u00c52<\/sup>); three nitrogen heteroatoms and three oxygen atoms give a multi-point hydrogen-bonding profile<\/td>\n<\/tr>\n
Hydrogen bond donors<\/th>\n1<\/td>\nthe amide N\u2013H group<\/td>\n<\/tr>\n
Hydrogen bond acceptors<\/th>\n4<\/td>\namide oxygen, lactam oxygen, furan oxygen, quinoline nitrogen<\/td>\n<\/tr>\n
Rotatable bonds<\/th>\n3<\/td>\na relatively rigid molecule \u2014 most of the skeleton is locked within the fused ring system<\/td>\n<\/tr>\n
Heavy atoms<\/th>\n25<\/td>\nthe molecule’s mass is distributed across an extensive, polycyclic core<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

A stereogenic center \u2014 which is absent here<\/h3>\n

Unlike modafinil<\/a>, where a stereogenic center on the sulfur atom necessitates distinguishing between enantiomers, coluracetam has no defined stereogenic center<\/strong> \u2014 the canonical InChI representation of this molecule contains no stereochemical layer. The carbon at position 4 of the furoquinoline system, to which the amide substituent is attached, lies in the plane of the conjugated ring system (a C=C double bond at this position), rather than in an sp3<\/sup> center bearing four different substituents. The practical consequence for the laboratory: the material does not require chiral separation when confirming identity.<\/p>\n

Nomenclature: the common name is younger than the development codes<\/h2>\n