Drug Database
TH

thiamine-cobaltichlorophyllate (Midoriamin)

✓ Approved

Nisshin Pharma · Small Molecule · Small Molecule

What is thiamine-cobaltichlorophyllate?

thiamine-cobaltichlorophyllate is a small molecule developed by Nisshin Pharma. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesMidoriamin
CompanyNisshin Pharma
Drug ClassSmall Molecule
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Nisshin Pharma

Therapeutic Indications

thiamine-cobaltichlorophyllate is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Gastrointestinal disordersDuodenal ulcer✓ Approved
Gastrointestinal disordersGastric ulcer✓ Approved

Related Research Articles

PubMedCase reports in neurology2026-07-25

Korsakoff Syndrome in a Late Adolescent with Wernicke Encephalopathy: A Case Report.

Bourcier Dax D, Holland Joanna J, Veysey Andrew A, Khan Naeem N et al.

Wernicke encephalopathy (WE) is a neurological emergency characterized by acute encephalopathy, oculomotor dysfunction, and ataxia, and may progress to Korsakoff syndrome - a disorder characterized by irreversible global episodic amnesia. Although classically linked to alcohol misuse, WE also arises in medical and psychiatric conditions associated with nutritional deficiency. We report an 18-year-old male with schizophrenia, non-adherent to antipsychotic treatment, who was admitted with disorganization, catatonia, and dehydration. After several days of minimal nutrition (including dextrose-containing fluids), oral lorazepam, and intramuscular olanzapine, he developed acute WE with worsening catatonia. Intravenous thiamine and continued lorazepam rapidly improved his level of consciousness. Laboratory testing revealed undetectable thiamine, and MRI findings were consistent with WE. Despite oral multivitamin supplementation, catatonia improved only after escalation to intravenous lorazepam and electroconvulsive therapy. As catatonia improved, symptomatology of schizophrenia emerged and improved significantly with paliperidone therapy. As schizophrenia symptoms improved, complete anterograde and partial retrograde amnesia, apathy, and anosognosia emerged, consistent with Korsakoff syndrome. He continued to meet diagnostic criteria at 3-year follow-up. This complex case demonstrates the importance of maintaining a suspicion of thiamine deficiency in patients with a history of nutritional depletion of greater or equal to 2 weeks. Prompt initiation and continuation of thiamine therapy while investigating and treating concurrent diagnoses can reduce the risk of WE and Korsakoff syndrome.

PMID 42499986
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PubMedFrontiers in pharmacology2026-07-24

Protection against cisplatin-induced acute kidney injury by hellgrammite extract: insights from comprehensive metabolomics.

Lin Kexin K, Lu Guangling G, Liu Rui R, He Yanmei Y et al.

Cisplatin (CP), a highly potent antineoplastic agent, is severely limited in clinical use by dose-limiting toxicities, particularly acute kidney injury (AKI). The hellgrammite (Hel), a kind of rare edible and medicinal insect, is known in Traditional Chinese Medicine (TCM) for its ability to tonify the qi and kidneys. However, its potential to ameliorate CP-induced AKI remains unexplored. We first evaluated the nutritional profile of Hel using high-performance liquid chromatography (HPLC) for amino acid composition analysis. Subsequently, a mouse model of CP-induced AKI was treated with different doses of Hel by gavage, then traditional pharmacology, and metabolomics were used to elucidate the effects and mechanism of Hel on CP-induced AKI mice. Hel effectively ameliorated CP-induced alterations in biochemical indicators and alleviated kidney pathological changes. Hel administration rectified the kidney metabolic disturbances induced by CP, involving alterations in 38 differential metabolites associated with glycerophospholipid metabolism, purine metabolism, nicotinate and nicotinamide metabolism, and thiamine metabolism. Hel confers renoprotection by reversing metabolic disorders in CP-induced AKI, revealing actionable targets for AKI intervention.

PMID 42494521
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PubMedChronic diseases and translational medicine2026-07-24

Plasma Exosome Metabolomics Reveal Stage-Specific Alterations in Elderly Women With Premetabolic and Metabolic Syndrome.

Qian Mengtao M, Nie Dan D, Gao Qianyi Q, Mo Xingbo X et al.

Metabolic syndrome (MetS) is a chronic disorder that poses a major threat to global health. Exosomes have emerged as promising biomarkers for diagnosing and monitoring chronic diseases. However, stage-specific alterations in the exosomal metabolome during MetS development remain poorly understood. This study aimed to characterize the plasma exosomal metabolome and explore candidate exosomal biomarkers in individuals with MetS. This study included 20 patients with MetS, 23 individuals with pre-MetS, and 45 healthy controls. Plasma exosomes were isolated and analyzed using untargeted liquid chromatography-mass spectrometry-based metabolomics. Differential metabolites were defined by a dual-threshold, that is, p < 0.05 from t-test and variable importance in projection > 1 from partial least squares discriminant analysis, with fold change indicating their expression changes. Further, we employed machine learning algorithms to predict MetS status. We identified 27 differential metabolites between the pre-MetS and control groups, mainly enriched in histidine metabolism and the tricarboxylic acid cycle. Of these, 12 metabolites were upregulated, and 15 were downregulated, with 1-methylhistidine and isocitrate playing central regulatory roles. Comparison between the MetS and control groups revealed 45 differentially expressed metabolites, mainly enriched in thiamine metabolism, including 13 upregulated and 32 downregulated. In the pre-MetS group, cladribine showed the highest area under the curve (AUC) (0.743, p < 0.05), whereas 3-methylxanthine yielded the largest AUC (0.714, p < 0.05) in the MetS group. Our study characterized stage-dependent alterations in the plasma exosome-derived metabolome in MetS and suggests that exosomal metabolomics may provide complementary molecular information on early MetS metabolic perturbations.

PMID 42494944
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PubMedBiochimie2026-07-22

Chronic oxidative stress leads to the accumulation of reversibly oxidised thiamine derivatives in tissues: effects of thiamine and cholecalciferol.

Parkhomenko Yu M YM, Veliky M M MM, Pavlova O S OS, Mezhenska O O OO et al.

There is limited data on oxidised thiamine (vitamin B1) derivatives in animal and human tissues. Some studies suggest that oxidative stress (OS) leads to their formation. This study aimed to estimate the proportion of reversibly oxidised (disulfide) thiamine derivatives in the total vitamin B1 pool in rat tissues exposed to various chronic OS forms, and to investigate the possibility of reducing these derivatives to a cyclic form. Rat models of thiamine deficiency and chronic alcoholism were used in experiments. The thiochrome method was used to analyse thiamine, with pretreatment of samples with a reducing agent and hydrolysis of thiamine phosphates performed separately under optimal conditions. The analysis of active and oxidised forms of vitamin B1, standard markers of OS and blood levels of 25(OH)D3 was performed in tissue samples. The corrective effect of thiamine and vitamin D3 supplementation was studied. In both models of OS, there was a decrease in the proportion of the active (cyclic) form of thiamine and a sharp increase in its oxidized (disulfide) forms, reaching levels of ∼50-70% of the total thiamine pool. High doses of thiamine (2 mg/kg) or vitamin D3 (2000 IU/kg) completely or partially normalized the situation with regard to OS indicators and also reduced the proportion of oxidized thiamine. Our results show that OS causes thiamine deficiency and tissue accumulation of thiamine disulfide derivatives. Red blood cell thiamine disulfide levels serve as a reliable marker of chronic OS, whereas a positive vitamin D deficiency test can mask actual vitamin B1 deficiency.

PMID 42480753
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PubMedInternal medicine (Tokyo, Japan)2026-07-21

Refeeding Syndrome Induced by Fursultiamine Infusion in Wernicke Encephalopathy: A Case Report.

Ishikawa Shotaro S, Ota Satoshi S, Nakazaki Natsuko N, Nagai Yoshio Y et al.

Wernicke encephalopathy is caused by thiamine deficiency, and treatment with high-dose thiamine is recommended for its management. We herein report the case of an older adult woman who developed refeeding syndrome after receiving intravenous fursultiamine. Although the patient's oral food intake was restricted to prevent refeeding syndrome, the total caloric load, including glucose contained in fursultiamine, exceeded the recommended amount. This case demonstrates that the caloric contribution of glucose present in fursultiamine should not be overlooked when treating Wernicke encephalopathy with high-dose parenteral fursultiamine.

PMID 42476772
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PubMedNature communications2026-07-21

Towards an enzyme cascade synthesis of the bulk chemical acrylic acid.

Zhao Haodong H, Wang Chunying C, Zhang Shiqing S, Wang Qian Q et al.

Acrylic acid is a bulk chemical predominantly produced via fossil-based processes. Here, we repurpose and engineer a thiamine diphosphate (ThDP)-dependent enzyme to catalyze direct H2PO4- elimination from dihydroxyacetone phosphate (DHAP) for acrylic acid synthesis. Quantum chemical calculations reveal the catalytic mechanism involving isomerization, enol-ThDP intermediate formation, H2PO4- elimination, and hydrolysis. Using an automated high-throughput screening platform, we perform directed evolution and obtain a 13.6-fold improved variant, designated acrylic acid synthase (AAS). We establish an enzymatic methanol-to-acrylic acid (MAAP) pathway, achieving a titer of 4.3 g L-1, a productivity of 268.9 mg L-1 h-1, and 99.5% conversion. This work establishes a high-efficiency biomanufacturing paradigm for bulk acrylic acid, and expands the catalytic repertoire of ThDP-dependent enzymes for sustainable one-carbon conversion.

PMID 42477336
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