Drug Database
KD

KD2-305 (KD2305 / KD 2305)

✓ Approved

Meiji Holdings · Recombinant Proteins · Recombinant Proteins

What is KD2-305?

KD2-305 is a recombinant proteins developed by Meiji Holdings. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesKD2305, KD 2305
CompanyMeiji Holdings
Drug ClassRecombinant Proteins
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Meiji Holdings

Therapeutic Indications

KD2-305 is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersFactor IX deficiency✓ Approved
Congenital, familial and genetic disordersFactor VIII deficiency✓ Approved

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Cockell Scarlet S, Harris Sean M SM, Morgan Rachel K RK, Patti Gary J GJ et al.

Dementia is a public health challenge and exposures likely contribute to risk, though many have not been evaluated. We screened chemicals for enrichment with dementia genes and related pathways. We obtained gene lists from Agora and the Comparative Toxicogenomics Database (CTD) for 1008 chemicals and nine dementia-related pathways (e.g., Alzheimer's disease, tauopathies). We tested pairwise chemical-dementia gene enrichment using Fisher exact tests and proportional reporting ratios (PRRs), accounting for multiple comparisons with false discovery rate (FDR < 1 × 10-6). Of the chemicals tested, 817 (81.1%) were enriched for at least one dementia pathway and 71 with all nine pathways, including benzo(a)pyrene, ethanol, paraquat, and particulate matter. We observed 295 chemicals enriched for Alzheimer's disease, including sodium arsenite (PRR = 57.9) and 305 enriched for tauopathies, including bisphenol A (PRR = 37.7). We identified chemicals enriched for dementia pathways, suggesting broad classes of chemicals contribute to dementia.

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PubMedThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2026-08-24

Gender Disparity in Academic Gastroenterology in Türkiye: A Nationwide Bibliometric Analysis.

Bilican Gülden G, Haas Stephan L SL, Uzar Hanife H, Kalkan Çağdaş Ç

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Diabetes and neurodegeneration in cognitively unimpaired older adults: implications for cognition.

Tsiknia Amaryllis A AA, Tennant Victoria R VR, Davison Marylan M, Nandy Rajesh R et al.

Type 2 diabetes mellitus is associated with cognitive impairment and greater Alzheimer's disease risk, with cross-sectional studies suggesting that this is driven by neurodegeneration and vascular changes. Longitudinal studies, however, report similar rates of total brain atrophy over time in diabetic and non-diabetic adults. We recently showed that diabetes-related neurodegeneration in cognitively unimpaired adults is regional and may not be evident in longitudinal studies of global brain atrophy. The mechanisms driving diabetes-related neurodegeneration are unknown; glycemic control may play an important role but the relative influence of Alzheimer's and cerebrovascular pathology is unclear. Here, we longitudinally examined regional patterns of cortical thinning associated with diabetes and glycemic control over nearly 3 years. We controlled for Alzheimer's disease neuropathology and white matter hyperintensity burden. We also examined whether subsequent changes in hemoglobin A1c (HbA1c) levels correlated with rates of cortical thinning in diabetes-associated regions and tested whether faster cortical thinning in diabetes-relevant regions mediated a relationship between diabetes and decline in cognitive performance. Among 1,298 cognitively unimpaired participants (mean age=65.0 years, 305 diabetic, 869 female) from the Health and Aging Brain Study-Health Disparities cohort who completed baseline and follow-up MRI scans, we used linear mixed-effects models to examine the relationship between diabetes and cortical thickness changes across 34 brain regions, controlling for socioeconomic factors and comorbidities. We further adjusted for amyloid-PET, tau-PET, white matter hyperintensities, and APOE ε4 carrier status. We also examined associations between baseline and longitudinal HbA1c levels and cortical thinning rates in diabetes-related regions in the whole sample and separately in diabetic and non-diabetic participants. P-values were corrected using the false discovery rate method. Path analysis tested whether diabetes-related cortical thinning mediated the relationship between diabetes and decline in cognitive performance. Diabetic participants exhibited faster cortical thinning in seven frontal, parietal, and occipital regions (-0.060≤βs≤-0.046, corrected Ps<0.017). Associations remained unchanged after accounting for socioeconomic factors, comorbidities, amyloid, tau, white matter hyperintensities, and APOE ε4. Higher baseline HbA1c predicted faster thinning in diabetes-vulnerable regions (corrected Ps<0.032), independent of subsequent HbA1c changes. Diabetes was associated with faster decline in processing speed (β=-0.022, P=0.033), with cortical thinning in diabetes-related regions mediating approximately 13% of this effect (indirect effect β=-0.034, P=0.019). Diabetes-related cortical thinning in cognitively unimpaired older adults follows a regional pattern independent of Alzheimer's and cerebrovascular pathology and partially mediates accelerated decline in processing speed. Chronic hyperglycemia may contribute to diabetes-related neurodegeneration, regardless of subsequent short-term changes in glycemic control.

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Nishikawa Yusuke Y, Fujimoto Ai A, Hayashi Yorihito Y, Tanaka Junji J et al.

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