Corti

At a glance

Pricing

Enterprise.

HIPAA

Not disclosed

SOC 2

Not disclosed

EHRs

—

Founded

—

HQ

DK

Bottom line

Real-time ambient + triage + decision support during encounter.

Free tier available.

Overview

Pricing

What it costs

Free tier only; no paid plans publicly disclosed.

Source: vendor pricing page. Verified May 23, 2026.

Peer-reviewed coverage

What the literature says

5 peer-reviewed studies indexed on PubMed evaluate Corti in clinical contexts. The most relevant are shown below, ranked by editorial relevance score combining title match, study design, recency, and journal tier.

Pharmacological activation of GPX4 by selenomethionine attenuates cisplatin-induced ototoxicity and hearing loss.

Li Z, Hu R, Deng W, et al.· Biochem Pharmacol· 2026

Cisplatin, an extensively used and effective antineoplastic agent for treating various malignancies, is well known for its ototoxicity. However, clinical treatments for ototoxicity remain limited. In this study, we investigated the protective role of selenomethionine (SeMet), an organic selenium compound, against cisplatin-induced ototoxicity. Our results demonstrated that SeMet effectively elevated cell viability and alleviated hair cells (HCs) loss in cisplatin-treated House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and cochlear explants in vitro and partially restored cisplatin-induce…

Unraveling Endocannabinoid Signaling Pathways in Cisplatin-Induced Ototoxicity.

Palaniappan S, Tisi A, Di Meo C, et al.· FASEB J· 2026

Cisplatin-induced ototoxicity is a detrimental side effect of chemotherapy leading to hearing loss, for which no treatments are currently available. Despite the growing recognition of the endocannabinoid (eCB) system (ECS) as a significant contributor to different physiological and pathological processes, its role in hearing remains poorly investigated. To fill this knowledge gap, we performed a molecular profiling of the ECS in auditory hair cell (HC)-like UB/OC1 cells derived from the mouse organ of Corti (OC), demonstrating the presence of the main eCBs-binding receptors and metabolic enzy…

Baicalin attenuates cisplatin-induced cochlear hair cell damage by modulating the ROS-p38 MAPK signaling pathway.

Zhang Q, Wang Y, Zhang C, et al.· Front Cell Dev Biol· 2026

Cisplatin-induced ototoxicity remains a major clinical challenge in chemotherapy, with limited pharmacological strategies available to prevent auditory damage. In this study, we explored the protective potential of baicalin, a flavonoid compound, against cisplatin-triggered cochlear injury. In vivo, baicalin was administered to C57BL/6 mice prior to cisplatin treatment. Auditory function was assessed using auditory brainstem response (ABR) and distortion product otoacoustic emission measurements, and cochlear hair cell integrity was examined. In vitro, both House Ear Institute-Organ of Corti…

Clotrimazole-Mediated Autophagy to Protect Against Cisplatin-Induced Ototoxicity via the AMPK/mTOR/TFEB Pathway in Mice.

Jiang Y, Li Z, Dong W, et al.· Antioxid Redox Signal· 2026

Cisplatin is an effective chemotherapeutic agent, but its clinical use is limited by dose-dependent ototoxicity that leads to irreversible sensorineural hearing loss. Accumulating evidence implicates impaired autophagy-lysosomal homeostasis in cisplatin-induced ototoxicity. Transcription factor EB (TFEB), a master regulator of autophagy and lysosomal biogenesis, represents a promising therapeutic target. Clotrimazole, an FDA-approved antifungal drug with emerging cytoprotective properties, has not been investigated for its potential to mitigate cisplatin-induced ototoxicity. We evaluated the…

Long-term restoration of auditory function in a DFNA2 mouse model by adenine base editing.

Kong Y, Zhang Y, Xie E, et al.· EMBO Mol Med· 2026

Hereditary hearing loss, the most prevalent genetic sensory disorder, lacks approved pharmacological therapies and represents a compelling target for gene correction. Pathogenic variants in KCNQ4 account for ~9.5% of autosomal dominant nonsyndromic cases. Prior gene-editing strategies disrupting mutant alleles have failed to achieve durable auditory rescue. Here we employed a knock-in mouse model harboring the human KCNQ4 c.961 G > A (p.G321S) mutation to evaluate precise base editing. Dual-AAV delivery of the adenine base editor ABE8e achieved 21.4-28.9% correction in th…

See all on PubMed