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aviptadil + phentolamine mesylate (Invicorp / VIP, Senetek / Resurgam)

✓ Approved

Johnson & Johnson Services, Inc. · VIPR1 · Small Molecule

What is aviptadil + phentolamine mesylate?

aviptadil + phentolamine mesylate is a small molecule developed by Johnson & Johnson Services, Inc.. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesInvicorp, VIP, Senetek, Resurgam
CompanyJohnson & Johnson Services, Inc.
Drug ClassSmall Molecule
Molecular TargetVIPR1
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Johnson & Johnson Services, Inc.

Mechanism of Action

Molecular Targets

aviptadil + phentolamine mesylate acts on 1 molecular target:

VIPR1vasoactive intestinal peptide receptor 1 (PACAP-R2, V1RG)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

aviptadil + phentolamine mesylate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Reproductive system and breast disordersErectile dysfunction✓ Approved

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PubMedMolecules (Basel, Switzerland)2026-10-16

Coffee Husk-Derived Activated Carbon for the Adsorptive Removal of Imatinib Mesylate from Water: Kinetic, Isotherm, Thermodynamic, and DFT Studies.

Párraga-García Vivian V, Chiquito Jeniffer J, Montero-Calderón Carolina C, Manangon-Perugachi Lucia E LE et al.

Coffee husk-derived activated carbon prepared by H3PO4 chemical activation was investigated for the removal of imatinib mesylate from aqueous solutions. Structural and chemical characterization using N2 physisorption, SEM, FTIR, Raman spectroscopy, and thermogravimetric analysis revealed a porous carbon matrix containing oxygenated functional groups and a defective turbostratic structure. The adsorption behavior was evaluated through batch experiments by examining the effects of pH, adsorbent dosage, particle size, contact time, and initial drug concentration. Under optimized conditions (300 µm particle size, 0.6 g adsorbent dosage, and pH 6), imatinib mesylate removal reached 97.9%, with equilibrium achieved within 60 min. The adsorption kinetics followed the pseudo-second-order model (R2 = 0.946-0.984), while equilibrium data were best described by the Sips isotherm model (R2 > 0.99), indicating adsorption on a heterogeneous surface. Density functional theory calculations confirmed the contribution of oxygen-containing groups, with carboxyl-functionalized carbon exhibiting the strongest interaction with imatinib mesylate (-105.3 kJ mol-1). These findings highlight the potential of coffee husk-derived activated carbon as a sustainable adsorbent for pharmaceutical contaminant removal.

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Exploiting Neosartorya (Aspergillus) fischeri antifungal protein 2-defined fungal targets for drug repurposing against Candida albicans.

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Invasive fungal infections caused by Candida albicans remain major clinical challenges because of the limited therapeutic options, toxicity, and emerging resistance. Drug repurposing offers a promising strategy to accelerate antifungal discovery by leveraging existing compounds with known safety profiles. In this study, we applied a structure-based drug repurposing approach guided by the antifungal protein Neosartorya (currently Aspergillus) fischeri antifungal protein 2 (NFAP2), which targets fungus-specific intracellular proteins, including glutamate decarboxylase, mitochondrial ATP synthase subunit alpha, and enolase. NFAP2-associated binding pockets were identified and used to virtually screen approved clinically investigated compounds. Selected candidates were further evaluated by molecular docking, followed by in vitro antifungal susceptibility testing and interaction analysis with conventional antifungal agents. In vivo toxicity and therapeutic efficacy were assessed using a Galleria mellonella infection model. Despite predicted binding affinities, most repurposed compounds exhibited limited antifungal activity in vitro, highlighting a disconnect between in silico predictions and biological efficacy. Among the tested compounds, dihydroergocristine mesylate (DHEC) and meclizine dihydrochloride exhibited measurable antifungal effects. Notably, DHEC demonstrated pronounced synergistic interactions with amphotericin B, resulting in near-complete growth inhibition in vitro. In vivo, DHEC + amphotericin B induced no detectable toxicity and significantly improved host survival compared with either drug alone. These findings indicate that NFAP2-guided structure-based drug repurposing can identify compounds targeting fungus-specific vulnerabilities. However, antifungal activity depends on factors beyond binding affinity. Our results highlight integrating computational screening with experimental validation and support repurposed compounds as adjuvants in combination therapies to enhance antifungal efficacy and translational potential.Invasive fungal infections caused by Candida albicans remain a major clinical challenge due to limited therapeutic options, toxicity, and emerging resistance. Drug repurposing offers a promising strategy to accelerate antifungal discovery by leveraging compounds with known safety profiles. A structure-based repurposing framework guided by the antifungal protein NFAP2, which targets fungus-specific intracellular proteins, is presented. Using these biologically informed targets, clinically relevant compounds with antifungal and adjuvant potential were identified. Predicted binding affinity alone did not reliably translate into antifungal activity, highlighting the need for integrated computational and experimental approaches. Notably, dihydroergocristine mesylate (DHEC) showed strong synergistic effects with amphotericin B, resulting in near-complete growth inhibition and improved host survival in vivo. These findings highlight the potential of repurposed compounds as adjuvants and support combination-based strategies targeting fungal-specific vulnerabilities. Furthermore, this work provides a framework for the future development of DHEC-inspired antifungal adjuvant strategies.

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PubMedClinical case reports2026-10-04

Pediatric Pheochromocytoma With Rapid Cyclic Blood Pressure Fluctuations: A Case Report.

Yamazaki Katsuaki K, Maeda Chika C, Morikawa Kaori K, Okamoto Naomi N

Cyclic blood pressure fluctuations in pheochromocytoma are extremely rare, and previously reported cases have been limited to adults. We report a 5-year-old boy with von Hippel-Lindau disease and a left adrenal pheochromocytoma who developed rapid cyclic blood pressure fluctuations immediately after tracheal intubation. Despite preoperative doxazosin (titrated from 0.5 to 3 mg/day over 27 days) and fluid loading, systolic blood pressure oscillated between 50 and 150 mmHg at approximately 7-min intervals after tracheal intubation. The fluctuations were independent of surgical manipulation and refractory to phenylephrine and phentolamine. Plasma norepinephrine was markedly elevated before tumor manipulation. After tumor resection, profound vasoplegic hypotension required high-dose norepinephrine, epinephrine, and vasopressin; hemodynamics gradually stabilized, and all vasoactive agents were discontinued on postoperative Day 3. This case demonstrates that pediatric pheochromocytoma can develop cyclic blood pressure fluctuations similar to those in adults and underscores the importance of individualized preoperative α-blockade and strict postoperative hemodynamic management after tumor resection.

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MINOS1-mediated mitochondrial remodeling: A critical regulator of apoptosis in hypoxic intestinal epithelium.

Yuan Jianlin J, Jian Chuanhui C, Li Xiaokai X, Li Xuemin X et al.

Intestinal epithelial cells (IECs) are highly vulnerable to mitochondrial dysfunction and lethal apoptosis under severe hypoxic stress. However, the upstream genetic determinants governing mucosal redox resilience remain poorly defined. To investigate the mechanisms of intestinal epithelial cell apoptosis under cobalt chloride (CoCl2)-induced hypoxic conditions, we established a CoCl2-induced lethal hypoxia model in IPEC-J2 cells and performed a genome-wide CRISPR-Cas9 screen. This screen identified MINOS1 as an essential gene for tolerance to CoCl2-induced hypoxic cell death. Systematic cell phenotyping and transcriptomic analyses revealed that CoCl2 exposure triggers robust intrinsic apoptosis and oxidative stress, whereas MINOS1 ablation remodels the basal transcriptomic landscape to establish an adaptive pro-survival state. Ultrastructural observation via transmission electron microscopy and subcellular functional assays demonstrated that MINOS1 deficiency eliminates canonical crista junctions (CJs) and induces distinctive concentric, "onion-like" remodeling of the inner mitochondrial membrane. Under severe hypoxia, MINOS1-knockout (KO) enterocytes retained stable mitochondrial membrane potential (ΔΨm), suppressed pathological mitochondrial permeability transition pore (mPTP) opening, sustained antioxidant enzyme (SOD and CAT) activities, and abrogated intracellular ROS accumulation and lipid peroxidation. Pharmacological intervention with the mitochondria-targeted antioxidant Mitoquinone mesylate precisely phenocopied the cytoprotective phenotype of MINOS1 ablation, confirming a mitochondria-dependent redox regulatory mechanism. Crucially, subcellular fractionation assays verified that remodeled concentric mitochondrial membranes form a unique topological barrier that physically sequesters cytochrome c within mitochondria, blocking its cytosolic release and subsequent activation of caspase-9 and caspase-3. Accordingly, MINOS1-deficient enterocytes tolerate extreme hypoxic stress by structurally uncoupling mitochondrial oxidative stress from downstream apoptotic execution. Collectively, these findings establish MINOS1-dependent cristae topology as a fundamental biophysical gatekeeper of intestinal mucosal redox homeostasis, providing a novel structure-targeted therapeutic strategy for hypoxia-associated intestinal disorders.

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PubMedBMJ open2026-09-28

Regional citrate anticoagulation combined with nafamostat mesylate for continuous kidney replacement therapy in septic acute kidney injury patients: protocol for a prospective, three-arm, randomised controlled study (RCNM-CKRT).

Xu Qing Q, Zou Hongxia H, Zhou Zhifeng Z, Fu Ping P et al.

Extracorporeal circuit (EC) clotting remains a major challenge in continuous kidney replacement therapy (CKRT). While regional citrate anticoagulation (RCA) is recommended first-line, nafamostat mesylate (NM) offers an alternative with potential anti-inflammatory benefits. This trial aims to compare the effects of RCA, NM and their combination on EC lifespan during CKRT in critically ill acute kidney injury (AKI) patients with sepsis. This is a single-centre, prospective, three-arm, open-label, randomised controlled trial. Critically ill adult patients with AKI with sepsis requiring CKRT will be enrolled. Participants will be randomly assigned (1:1:1) to receive RCA, NM or combined RCA+NM anticoagulation. The primary outcome is EC lifespan. Secondary outcomes include EC survival rates, patient mortality, inflammatory biomarker levels and safety events (eg, bleeding, citrate accumulation). The sample size of 258 patients (86 per group) was calculated to detect a significant difference in the primary outcome with 90% power. Analysis will follow the intention-to-treat principle, using Kaplan-Meier survival analysis and Cox regression for the primary outcome. The RCNM-CKRT trial has been approved by the Biomedical Ethics Review Committee of West China Hospital, Sichuan University. We plan to present the results of our research at an international conference and publish in a peer-reviewed journal. The study data will be available on request, ensuring transparency and accessibility.Trial registration number:ChiCTR2600121436; Pre-results.

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Well-regulated trophoblast proliferation, migration, invasion, and cell turnover are essential for normal placental development in humans and rodents. Given the established role of oxidative stress in placentation and the redox activity of iron, we investigated whether ferroptosis-associated redox signaling contributes to trophoblast function and placental development. Placental iron profiling revealed significantly elevated total and ferrous iron levels in first-trimester human villi compared with term placentas, accompanied by the transcript levels of several iron uptake- and reduction-related genes, including TFRC, DMT1, ZIP8, STEAP3, and STEAP4, which were elevated in first-trimester villi. Murine placentas also exhibited gestational changes in iron abundance and iron-homeostasis-related gene expression. HO-1 protein abundance was highest during early gestation and declined thereafter, suggesting a potential association between heme degradation and gestational iron homeostasis. In contrast, placental labile iron pool (LIP) levels showed only modest, statistically nonsignificant changes across gestation, suggesting a relatively stable redox-active iron pool. Immunofluorescence analyses demonstrated spatially distinct expression of ferroptosis-associated regulators, with ACSL4 enriched in invasive trophoblast populations and GPX4 predominantly localized in surrounding decidual tissues, suggesting regional heterogeneity in ferroptosis-associated molecular features during placentation. Functional studies in HTR-8/SVneo trophoblast cells further demonstrated that mild ferroptosis-associated redox perturbation induced by low-dose erastin or ferrous iron enhanced trophoblast migration and invasion without overt cytotoxicity. These effects were attenuated by ferrostatin-1, deferoxamine mesylate (DFOM), or the mitochondria-targeted antioxidant MitoQ and were blunted following FTH1 and TFRC knockdown, indicating that trophoblast responsiveness depends on iron availability and ferroptosis-associated redox signaling. Importantly, these pro-invasive effects were preserved under physiologically relevant hypoxic conditions. Together, our findings support a model in which gestational changes in placental iron homeostasis are associated with ferroptosis-related molecular features, while experimentally induced iron-dependent redox signaling modulates trophoblast behavior. Rather than inducing overt ferroptotic cell death, sublethal iron-dependent redox perturbation may act as a signaling mechanism influencing trophoblast function during placental development.

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