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Last update 24 Mar 2025
AZD-1305
Last update 24 Mar 2025
Overview
Basic Info
Drug Type Small molecule drug |
Synonyms AZD 1305, AZD1305 |
Action blockers |
Mechanism L-type calcium channel blockers(Voltage-gated L-type calcium channel blockers), Nav1.5 blockers(Sodium channel protein type V alpha subunit blockers), hERG blockers(Voltage-gated potassium channel subunit Kv11.1 blockers) |
Therapeutic Areas |
Active Indication- |
Inactive Indication |
Originator Organization |
Active Organization- |
Inactive Organization |
Drug Highest PhaseDiscontinuedPhase 2 |
First Approval Date- |
Regulation- |
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Structure/Sequence
Molecular FormulaC22H31FN4O4 |
InChIKeyBLLNYXOLLAVTRF-UHFFFAOYSA-N |
CAS Registry872045-91-5 |
Related
14
Clinical Trials associated with AZD-1305NCT00957437
A Phase I, Randomised, Open, Single-centre Study to Evaluate the Pharmacokinetics of Different Extended-release Formulations of AZD1305 When Given as Single and Repeated Oral Doses to Healthy Male Volunteers
NCT00935025
A Single-center, Single-blind, Randomized, Placebo-controlled, Phase I Study to Assess the Safety, Tolerability and Pharmacokinetics After Single and Multiple Ascending Oral Doses of AZD1305 Extended-release Capsules in Healthy Male Japanese and Caucasian Subjects
EUCTR2009-009862-15-CZ
A double-Blind, Randomised, Placebo-Controlled, Multicentre, Dose-Escalating Study of AZD1305 Given Intravenoulsy for Cardioversion of Atrial Fibrillation
100 Clinical Results associated with AZD-1305
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100 Translational Medicine associated with AZD-1305
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100 Patents (Medical) associated with AZD-1305
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19
Literatures (Medical) associated with AZD-130501 Jul 2024EBioMedicine
Advancing drug development for atrial fibrillation by prioritising findings from human genetic association studies
Article
Author: Providencia, Rui ; Lambiase, Pier D ; Finan, Chris ; Schilling, Richard ; Floriaan Schmidt, Amand ; Kukendrarajah, Kishore ; Farmaki, Aliki-Eleni
BACKGROUND:
Drug development for atrial fibrillation (AF) has failed to yield new approved compounds. We sought to identify and prioritise potential druggable targets with support from human genetics, by integrating the available evidence with bioinformatics sources relevant for AF drug development.
METHODS:
Genetic hits for AF and related traits were identified through structured search of MEDLINE. Genes derived from each paper were cross-referenced with the OpenTargets platform for drug interactions. Confirmation/validation was demonstrated through structured searches and review of evidence on MEDLINE and ClinialTrials.gov for each drug and its association with AF.
FINDINGS:
613 unique drugs were identified, with 21 already included in AF Guidelines. Cardiovascular drugs from classes not currently used for AF (e.g. ranolazine and carperitide) and anti-inflammatory drugs (e.g. dexamethasone and mehylprednisolone) had evidence of potential benefit. Further targets were considered druggable but remain open for drug development.
INTERPRETATION:
Our systematic approach, combining evidence from different bioinformatics platforms, identified drug repurposing opportunities and druggable targets for AF.
FUNDING:
KK is supported by Barts Charity grant G-002089 and is mentored on the AFGen 2023-24 Fellowship funded by the AFGen NIH/NHLBI grant R01HL092577. RP is supported by the UCL BHF Research Accelerator AA/18/6/34223 and NIHR grant NIHR129463. AFS is supported by the BHF grants PG/18/5033837, PG/22/10989 and UCL BHF Accelerator AA/18/6/34223 as well as the UK Research and Innovation (UKRI) under the UK government's Horizon Europe funding guarantee EP/Z000211/1 and by the UKRI-NIHR grant MR/V033867/1 for the Multimorbidity Mechanism and Therapeutics Research Collaboration. AF is supported by UCL BHF Accelerator AA/18/6/34223. CF is supported by UCL BHF Accelerator AA/18/6/34223.
01 Jun 2018British Journal of Pharmacology
Human hepatocytes and cytochrome P450‐selective inhibitors predict variability in human drug exposure more accurately than human recombinant P450s
Article
Author: Lundahl, Anna ; Lindmark, Bo ; Andersson, Tommy B ; Isin, Emre M ; Kanebratt, Kajsa P
Background and Purpose:
Drugs metabolically eliminated by several enzymes are less vulnerable to variable compound exposure in patients due to drug–drug interactions (DDI) or if a polymorphic enzyme is involved in their elimination. Therefore, it is vital in drug discovery to accurately and efficiently estimate and optimize the metabolic elimination profile.
Experimental Approach:
CYP3A and/or CYP2D6 substrates with well described variability in vivo in humans due to CYP3A DDI and CYP2D6 polymorphism were selected for assessment of fraction metabolized by each enzyme (fmCYP) in two in vitro systems: (i) human recombinant P450s (hrP450s) and (ii) human hepatocytes combined with selective P450 inhibitors. Increases in compound exposure in poor versus extensive CYP2D6 metabolizers and by the strong CYP3A inhibitor ketoconazole were mathematically modelled and predicted changes in exposure were compared with in vivo data.
Key Results:
Predicted changes in exposure were within twofold of reported in vivo values using fmCYP estimated in human hepatocytes and there was a strong linear correlation between predicted and observed changes in exposure (r2 = 0.83 for CYP3A, r2 = 0.82 for CYP2D6). Predictions using fmCYP in hrP450s were not as accurate (r2 = 0.55 for CYP3A, r2 = 0.20 for CYP2D6).
Conclusions and Implications:
The results suggest that variability in human drug exposure due to DDI and enzyme polymorphism can be accurately predicted using fmCYP from human hepatocytes and CYP‐selective inhibitors. This approach can be efficiently applied in drug discovery to aid optimization of candidate drugs with a favourable metabolic elimination profile and limited variability in patients.
01 Oct 2017British Journal of Pharmacology
Predicting QRS and PR interval prolongations in humans using nonclinical data
Article
Author: Collins, T ; Mettetal, J ; Parkinson, J ; Chappell, M J ; Bergenholm, L ; Evans, N D
Background and Purpose:
Risk of cardiac conduction slowing (QRS/PR prolongations) is assessed prior to clinical trials using in vitro and in vivo studies. Understanding the quantitative translation of these studies to the clinical situation enables improved risk assessment in the nonclinical phase.
Experimental Approach:
Four compounds that prolong QRS and/or PR (AZD1305, flecainide, quinidine and verapamil) were characterized using in vitro (sodium/calcium channels), in vivo (guinea pigs/dogs) and clinical data. Concentration‐matched translational relationships were developed based on in vitro and in vivo modelling, and the in vitro to clinical translation of AZD1305 was quantified using an in vitro model.
Key Results:
Meaningful (10%) human QRS/PR effects correlated with low levels of in vitro Nav1.5 block (3–7%) and Cav1.2 binding (13–21%) for all compounds. The in vitro model developed using AZD1305 successfully predicted QRS/PR effects for the remaining drugs. Meaningful QRS/PR changes in humans correlated with small effects in guinea pigs and dogs (QRS 2.3–4.6% and PR 2.3–10%), suggesting that worst‐case human effects can be predicted by assuming four times greater effects at the same concentration from dog/guinea pig data.
Conclusion and Implications:
Small changes in vitro and in vivo consistently translated to meaningful PR/QRS changes in humans across compounds. Assuming broad applicability of these approaches to assess cardiovascular safety risk for non–arrhythmic drugs, this study provides a means of predicting human QRS/PR effects of new drugs from effects observed in nonclinical studies.
100 Deals associated with AZD-1305
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R&D Status
10 top R&D records. to view more data
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| Indication | Highest Phase | Country/Location | Organization | Date |
|---|---|---|---|---|
| Ventricular Dysfunction, Left | Phase 2 | Sweden | 01 Aug 2008 | |
| Atrial Fibrillation | Phase 2 | Denmark | 01 Mar 2008 | |
| Atrial Fibrillation | Phase 2 | Norway | 01 Mar 2008 | |
| Atrial Fibrillation | Phase 2 | Poland | 01 Mar 2008 | |
| Atrial Fibrillation | Phase 2 | Russia | 01 Mar 2008 | |
| Atrial Fibrillation | Phase 2 | Slovakia | 01 Mar 2008 | |
| Atrial Fibrillation | Phase 2 | Sweden | 01 Mar 2008 | |
| Atrial Flutter | Phase 2 | Denmark | 01 Jan 2008 | |
| Atrial Flutter | Phase 2 | Finland | 01 Jan 2008 | |
| Atrial Flutter | Phase 2 | Norway | 01 Jan 2008 |
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Clinical Result
Clinical Result
Indication
Phase
Evaluation
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Phase 2 | 228 | (AZD1305 Dose Group 1) | lknpobdzox(wonhsyjris) = zzqkfphild bwmyiqspqd (lhipgpugwt, ppmuytavmf - nrajzvfjpe) View more | - | 01 Feb 2012 | ||
(AZD1305 Dose Group 2) | lknpobdzox(wonhsyjris) = wtdsvckixk bwmyiqspqd (lhipgpugwt, lxbxkswpwd - kwwzkoinox) View more | ||||||
Phase 2 | 65 | (AZD1305 Group A and AZD1305 Group B) | baovhevabp(ugrtniumug) = tpzmvfjbga yffethhxes (ygiygpxhhl, lrcjrxgryl - jwyqlckjlu) View more | - | 26 Jan 2012 | ||
Placebo+AZD1305 (Placebo) | baovhevabp(ugrtniumug) = yihumgnqtn yffethhxes (ygiygpxhhl, ofgkwdjkcg - rzswrczegc) View more | ||||||
Phase 2 | 171 | leiqccpbqb(yflkmztufr) = hlsufpepqu zbsllikfvn (kpvoncwkcb ) View more | Negative | 01 Aug 2011 | |||
Phase 2 | 16 | (AZD1305 Dose 1 and Dose 2) | ptflzxegzg(mupgyulnnp) = imtghjocdl wdgxhszcee (gfkllujffw, smawwgbbsq - qvkvpkllzs) View more | - | 13 Jun 2011 | ||
Placebo (Placebo Dose 1 and Dose 2) | ptflzxegzg(mupgyulnnp) = ypfioaoaix wdgxhszcee (gfkllujffw, ztietbgkgw - kzozssuaql) View more |
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