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AZ

aztreonam lysine (Cayston / Corus 1020 / AZLI)

✓ Approved

Gilead Sciences, Inc. · Small Molecule · Small Molecule

What is aztreonam lysine?

aztreonam lysine is a small molecule developed by Gilead Sciences, Inc.. It is approved for therapeutic indications via inhaled.

Drug Profile

Brand NamesCayston, Corus 1020, AZLI
CompanyGilead Sciences, Inc.
Drug ClassSmall Molecule
RouteInhaled
StatusApproved
Sources: ClinicalTrials.gov, Gilead Sciences, Inc.

Therapeutic Indications

aztreonam lysine is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Infections and infestationsRespiratory tract infection✓ Approved
Infections and infestationsPneumonia pseudomonal✓ Approved
Respiratory, thoracic and mediastinal disordersBronchiectasisPhase III

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KDM4B (Lysine demethylase 4B), a histone lysine demethylase, exerts a crucial epigenetic regulatory role in the progression of numerous disorders by catalyzing demethylation reactions on target proteins. However, the precise biological function and molecular mechanism by which KDM4B regulates neurological deficits in ischemic stroke remains elusive. In this study, we employed a mouse middle cerebral artery occlusion/reperfusion (MCAO/R) model and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in HT22 neurons to mimic ischemic stroke. Targeted loss-of-function approaches were executed utilizing in vivo siRNA delivery and in vitro lentiviral shRNA transduction. The neuroprotective effects were systematically evaluated through infarct volume quantification, histopathological staining, and diverse sensorimotor behavioral tests. Furthermore, transcriptomic profiling (RNA-seq) coupled with molecular biology assays was performed to elucidate the downstream apoptotic cascades and key targets governed by KDM4B. Herein, we found that KDM4B is predominantly localized in neurons, with its expression significantly decreasing initially and then gradually increasing following ischemic stroke. Loss-of-function experiments demonstrated that KDM4B knockdown mitigated brain damage, attenuated tissue structure disruption, and improved sensorimotor dysfunctions in mice with ischemic stroke. Additionally, KDM4B knockdown protected neurons against OGD/R insult. Furthermore, KDM4B knockdown inhibited the expression of Bax and the activation of the pro-apoptotic caspase cascade (caspase-3/6/7/8/9), while upregulating the expression of the anti-apoptotic protein Bcl-2, thereby reducing neuronal apoptosis. Mechanistically, KDM4B knockdown is associated with an upregulation of Birc5 expression, which in turn inhibits apoptotic progression in neurons. These results demonstrate that KDM4B knockdown alleviates neurological deficits following ischemic stroke by inhibiting neuronal apoptosis, partially accompanied by Birc5.

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Author Correction: Histone H3 trimethylation at lysine 36 guides m6A RNA modification co-transcriptionally.

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