CAS 364-62-5 Metoclopramide - Analytical Products / Alfa Chemistry

CAT	APS364625
CAS	364-62-5
MDL Number	MFCD00211338
Synonyms	Metoclopramide, 4-Amino-5-chloro-N-[2-(diethylamino)ethyl]-2-methoxybenzamide
IUPAC Name	4-amino-5-chloro-N-[2-(diethylamino)ethyl]-2-methoxybenzamide
Molecular Weight	299.80
Molecular Formula	C14H22ClN3O2
EC Number	206-662-9
Canonical SMILES	CCN(CC)CCNC(=O)c1cc(Cl)c(N)cc1OC
InChI	InChI=1S/C14H22ClN3O2/c1-4-18(5-2)7-6-17-14(19)10-8-11(15)12(16)9-13(10)20-3/h8-9H,4-7,16H2,1-3H3,(H,17,19)
InChI Key	TTWJBBZEZQICBI-UHFFFAOYSA-N
REAXYS Number	1884366

Description	analytical standard
Accurate Mass	299.1401
Form	neat; gas chromatography (GC): suitable
Format	Neat
Grade	analytical standard
Size	100MG
Storage Conditions	2-8°C

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APS364625-1	100MG	Room Temperature	+20°C	Subcategory: Pharmaceutical and veterinary compounds and metabolites	Inquiry
APS364625-2	100MG	Room Temperature	2-8°C Fridge/Coldroom	API Family: Matrix - API Family See respective official monograph(s); Product Type: API; Subcategory: European Pharmacopoeia (Ph. Eur.)	Inquiry

Case Study

Metoclopramide Used for the Inhibition of CD93 Signaling in Leukemia Stem Cells

Riether, Carsten, et al. Cell reports 34.4 (2021).

Recent studies have uncovered a novel therapeutic application for metoclopramide, a well-known anti-emetic drug, in targeting leukemia stem cells (LSCs) in chronic myeloid leukemia (CML). CD93, a transmembrane protein highly expressed on LSCs but not on normal hematopoietic stem cells (HSCs), has been identified as a key regulator of self-renewal and proliferation in LSCs. CD93 signaling functions through its intracellular domain, activating a gene expression program via the transcriptional regulator SCYL1, independent of ligand binding.
In a high-throughput drug screen, metoclopramide emerged as a potent inhibitor of CD93-mediated signaling. Functional assays demonstrated that metoclopramide treatment significantly reduced the population of murine and human LSCs in vitro. In a murine model of CML, metoclopramide administration led to decreased expression of genes associated with stemness and cell cycle progression, suppressed LSC proliferation, and notably extended survival.
Importantly, metoclopramide's specificity for CD93-expressing LSCs, with minimal effect on normal HSCs, suggests a promising therapeutic window for its repurposing in CML treatment. These findings not only highlight CD93 as a novel and targetable LSC-specific pathway but also position metoclopramide as a candidate for differentiation therapy in hematologic malignancies.
This study underscores the potential of drug repurposing to accelerate the development of targeted leukemia therapies and establishes metoclopramide as a compelling inhibitor of LSC self-renewal via CD93 blockade.

Metoclopramide Used for the Suppression of Central Trigeminovascular Activation in Migraine Therapy

Dolgorukova, Antonina, et al. Neuroscience 425 (2020): 123-133.

Metoclopramide, traditionally employed as an antiemetic, has emerged as an effective abortive treatment for acute migraine due to its additional analgesic properties. While its clinical efficacy in migraine management is well established, the precise mechanism behind its anti-cephalalgic action has remained unclear.
This study investigates the role of metoclopramide in modulating trigeminovascular nociception, a key pathway in migraine pathophysiology. Using electrophysiological models in anesthetized rats, metoclopramide was administered via cumulative intravenous infusion (5 mg/kg per step, three steps, 30-minute intervals). The results showed a significant and dose-dependent suppression of both spontaneous and evoked firing of dura-sensitive second-order neurons in the trigeminocervical complex (TCC), with maximal reductions to 30% and 4% of baseline activity, respectively (p = 0.001).
Interestingly, metoclopramide did not affect neurogenic dural vasodilation, suggesting its anti-migraine action is centrally mediated rather than through peripheral vascular modulation. This central inhibition of TCC neuron excitability directly correlates with its therapeutic potential in migraine, distinguishing metoclopramide as a modulator of central nociceptive pathways rather than vasodilatory responses.
These findings provide a compelling neurophysiological basis for the anti-migraine efficacy of metoclopramide, positioning it as a dual-action therapeutic that effectively targets the central components of trigeminovascular activation implicated in migraine attacks.