Drug Database
CA

caffeine citrate (Cafnea)

✓ Approved

Phebra · Small Molecule · Small Molecule

What is caffeine citrate?

caffeine citrate is a small molecule developed by Phebra. It is approved for therapeutic indications via injectable (others) or oral (po).

Drug Profile

Brand NamesCafnea
CompanyPhebra
Drug ClassSmall Molecule
RouteInjectable (Others), Oral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Phebra

Therapeutic Indications

caffeine citrate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Respiratory, thoracic and mediastinal disordersApnoea✓ Approved

Related Research Articles

PubMedJournal of clinical apheresis2026-10-15

Apheresis in Children of Weight Under 7 kg-A Single Center Experience.

Rungsiprakarn Phassawan P, Wilson Bryan E BE, Rintoul Natalie E NE, Wild K Taylor KT et al.

Although apheresis techniques in children are well established, published experience with very low-weight children is limited. We reviewed 68 procedures performed in 19 children weighing less than 7 kg, including hematopoietic progenitor and T-cell collections and plasmapheresis. With significant modifications of standard techniques, all but one procedure was successfully and safely completed without serious citrate toxicity. Access was a major challenge. For plasmapheresis, the mean plasma volume removed was 1.2 × total plasma volume, but the mean total blood processed was 1.74 × total blood volume (TBV). For collections, the mean number of whole blood volumes processed was 4.1 × TBV. For T cell collections, the median CD3+ yield was 243.6 × 106/kg. For HPC collections, the median CD34+ cell yield was 14.8 × 106/kg. Mean durations for collections and plasmapheresis were 247.00 and 120.67 min, respectively. Of the CBC parameters, only platelet count was significantly lower after collections.

PMID 42875967
Read full article →
PubMedPharmacological reports : PR2026-10-15

GLS2 reshapes glycolytic metabolism and bioenergetic homeostasis in glioblastoma cells.

De Los Santos-Jiménez Juan J, Campos-Sandoval José A JA, Sudderth Jessica J, Zacharias Lauren G LG et al.

Glioblastoma (GBM) exhibits extensive metabolic reprogramming, including glucose and glutamine (Gln) addiction, with Gln being converted into glutamate by glutaminase, encoded by the GLS and GLS2 genes. GLS2 acts as a context-dependent tumor suppressor, although the underlying mechanisms remain poorly understood. GLS2 is silenced in GBM, and we previously showed that its re-expression modulates pyruvate dehydrogenase (PDH) activity and tricarboxylic acid cycle (TCAC) metabolism, suggesting a distinct metabolic rewiring associated with its tumor-suppressive function. LN229 and T98G GBM cell lines were used as experimental models. Metabolomic profiling by liquid chromatography-mass spectrometry was performed to compare changes in central metabolic pathways following GLS2 or GLS overexpression. Glutaminase and PDH enzymatic activities were measured, and Western blotting was performed to assess GLS, GLS2, and PDHA1 protein levels and PDHA1 phosphorylation. A Seahorse analyzer was employed to quantify real-time ATP production derived from glycolysis and oxidative phosphorylation. Overexpression of GLS2, but not GLS, in LN229 cells caused the accumulation of TCAC-related metabolites, except for citrate, whose depletion is attributed to GLS2's effect on PDH phosphorylation, causing reduced PDH activity. This was accompanied by decreased levels of several acyl-carnitines. Furthermore, GLS2 induced the accumulation of glucose/fructose, while reducing levels of glucose-6-phosphate and pentose-phosphates, consistent with altered glycolysis. GLS2 also diminished the ATP/AMP ratio, confirmed by a reduced ATP synthesis rate, particularly glycolytic ATP, whereas mitochondrial ATP production remained unaltered. GLS2 exerts an isoenzyme-specific effect on Gln and glucose metabolism in GBM, likely modulating the glycolysis/pentose-phosphate pathway (PPP)-TCAC-axis.

PMID 42875721
Read full article →
PubMedDrugs2026-10-15

Metformin Lowers Fasting Hyperglycemia by Increasing Glucose Clearance in People with Moderately Controlled Type 2 Diabetes.

Kahl Sabine S, LaMoia Traci E TE, Jonuscheit Marc M, Heilmann Geronimo G et al.

Metformin is the most frequently prescribed antidiabetic drug worldwide; however, the mechanism by which it lowers blood glucose remains incompletely understood. The objective of this study was to examine the effects of metformin on whole-body and specifically on hepatic glucose and energy metabolism in type 2 diabetes. This open repeated-measures pilot study examined this question using Positional Isotopomer NMR Tracer Analysis (PINTA) to assess rates of endogenous glucose production (VEGP), hepatic pyruvate carboxylase flux (VPC), and citrate synthase (VCS) flux in 16 men with moderately controlled type 2 diabetes (T2D; BMI 30 ± 3 kg/m2, HbA1c 8.4 ± 1.4%) undergoing two examination days with (M+; 1 g twice daily) and without metformin (M-) treatment. Hepatic ATP and glycogen concentrations were quantified by 31P/13C magnetic resonance spectroscopy. M+ reduced fasting glycemia by 18%, which could mostly be attributed to a 24% increase in rates of whole-body glucose clearance. Surprisingly, these changes were accompanied by a 58% increase in VPC and a 34% increase in VCS, due to a 26% increase in plasma glucagon concentrations. The increase in VPC was offset by reductions in the contributions of glycerol conversion to glucose resulting in no change in VEGP. Metformin decreased hepatic ATP content by 16% and increased plasma GDF-15 concentrations, but did not alter rates of net hepatic glycogenolysis. Metformin treatment in male individuals of European ancestry with moderately controlled T2D decreases blood glucose concentrations by increasing rates of whole-body glucose clearance. Metformin further inhibits glycerol-derived gluconeogenesis, which is consistent with complex IV, not complex I, being the molecular target of metformin action. ClinicalTrials.gov ( https://clinicaltrials.gov/ ): NCT04088851.

PMID 42875657
Read full article →
PubMedBiological psychiatry. Cognitive neuroscience and neuroimaging2026-10-14

Caffeine Consumption and Adolescent Mental Health: The Role of Sleep and Brain Structure.

Zheng Jiayi J, Rakesh Divyangana D

Caffeine is a widely consumed psychoactive substance, with use beginning during adolescence, a sensitive period of neurodevelopment. Despite its widespread, unregulated use, links between caffeine consumption and adolescent brain structure and mental health remain poorly understood. We examined the association between caffeine intake and brain structure in 9632 adolescents aged 9-11 years. Caffeine consumption (intake of coffee, tea and soft drinks) and mental health were assessed via self-report. Cortical thickness and surface area were derived from structural MRI scans. Linear mixed-effects models tested associations between caffeine intake and brain measures. Structural equation modeling was used to test whether sleep duration and brain structure mediated the association between caffeine intake and mental health outcomes assessed at the 6-month and 18-month follow-up. Higher total caffeine intake was associated with lower total cortical surface area (B=-0.03,SE=0.01,p=.001) and lower surface area in 22 regions across four lobes, driven largely by soft drink consumption, with some additional associations emerging for coffee and espresso intake with cortical thickness. All associations were evident at consumption levels as low as one cup per week. Shorter sleep duration and lower surface area sequentially mediated the association between higher caffeine intake and greater mental health problems in the future. Findings highlight the need for evidence-based guidelines on adolescent caffeine consumption to support neurodevelopment and mental health.

PMID 42874917
Read full article →
PubMedPlastic and reconstructive surgery2026-10-14

Optimizing Concentrated Growth Factor Therapy: Sodium Citrate Reduces Pain in Hair Loss Treatment.

Pan Wenxing W, Chen Xinyi X, Li Haoyang H, Miao Zechen Z et al.

Androgenetic alopecia (AGA) is a prevalent condition causing significant psychosocial distress. While concentrated growth factor (CGF) therapy has emerged as a promising regenerative treatment, the choice of anticoagulant remains a critical but underexplored variable that may affect the growth factor release, and patient experience. To compare the efficacy, procedural pain, and patient satisfaction of CGF prepared with sodium citrate, heparin sodium, or no anticoagulant in patients with AGA. This phase 2, multicenter, single-blind, randomized controlled trial enrolled 267 patients aged 18 to 50 years across three tertiary hospitals in China. Participants were randomized 1:1:1 to receive CGF prepared without anticoagulant (Group A), with 3.2% sodium citrate (Group B), or with heparin sodium (Group C). All patients underwent five intradermal injection sessions over 12 months. Primary endpoints included injection-related pain (VAS) and changes in hair density at 3, 6, and 12 months. Injection pain was significantly lower in Group B (P < 0.001). At 6 and 12 months, Group B demonstrated significantly greater hair density increases and higher rates of ≥50% subjective clinical improvement (P < 0.001). In vitro analysis confirmed that sodium citrate best preserved growth factor levels and platelet function. Overall satisfaction and willingness for re-treatment were highest in Group B (87.6%). Sodium citrate provided the most favorable balance of procedural tolerability, delivery reliability, and clinical efficacy. These findings support sodium citrate as the preferred anticoagulant for CGF preparation in AGA, while confirmation in broader populations and phase 3 trials is warranted.

PMID 42873090
Read full article →
PubMedJournal of enzyme inhibition and medicinal chemistry2026-10-14

Research progress on ATP-citrate lyase and its inhibitors: a metabolic-epigenetic perspective.

Liu Qinglin Q, Sun Hongbin H, Dai Liang L

ATP-citrate lyase (ACLY) is a key enzyme in cellular metabolism that catalyses the cleavage of citrate to produce acetyl coenzyme A (acetyl-CoA), thereby bridging energy metabolism and epigenetic regulation. Acetyl-CoA serves as a common substrate for de novo lipogenesis (DNL) and histone acetylation. Aberrant ACLY activity is closely associated with various pathological conditions, including metabolic diseases, Immune-mediated inflammatory diseases (IMIDs), cancer, and neurodegenerative diseases, positioning ACLY as an important therapeutic target for these diseases. However, existing inhibitors face challenges such as insufficient selectivity and limited clinical efficacy and off-target effects. This review systematically summarises the molecular mechanisms and pathological significance of ACLY within the overarching framework of its dual metabolic-epigenetic functions, from three perspectives, namely its structure and function, disease relevance, and inhibitor development and optimisation strategies, aiming to provide a theoretical foundation for precision therapies targeting ACLY.

PMID 42875375
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about caffeine citrate