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amlodipine + celecoxib (Consensi / KIT 302 / KIT302)

✓ Approved

Burke Pharmaceutical · CACNA1C · Small Molecule

What is amlodipine + celecoxib?

amlodipine + celecoxib is a small molecule developed by Burke Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesConsensi, KIT 302, KIT302
CompanyBurke Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetCACNA1C, PTGS2
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Burke Pharmaceutical

Mechanism of Action

Molecular Targets

amlodipine + celecoxib acts on 2 molecular targets:

CACNA1Ccalcium voltage-gated channel subunit alpha1 C (NEDHLSS, CACH2)
PTGS2prostaglandin-endoperoxide synthase 2 (hCox-2, PHS-2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

amlodipine + celecoxib is developed for 3 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved
Musculoskeletal and connective tissue disordersMusculoskeletal pain✓ Approved
Renal and urinary disordersRenal failurePreclinical

Related Research Articles

PubMedFrontiers in pain research (Lausanne, Switzerland)2026-10-15

Yaobitong plus celecoxib for low back pain: a Chinese multicenter cohort and network pharmacology study.

Gong Huahui H, Lu Chenxing C, Guo Zhanghao Z, Wu Min M et al.

Yaobitong capsule is frequently co-administered with celecoxib for low back pain in China, but its incremental effectiveness and safety in routine clinical practice remain uncertain. We compared Yaobitong plus celecoxib with celecoxib alone and explored potential biological mechanisms. This multicenter retrospective cohort study included Chinese outpatients with low back pain treated at 3 hospitals. After 1:1 propensity score matching, 150 patients receiving Yaobitong plus celecoxib were compared with 150 receiving celecoxib alone. The primary outcome was the change in the Oswestry Disability Index (ODI) at 1 month. Secondary outcomes included pain, lumbar function, clinically meaningful response, rescue analgesic use, treatment escalation, and adverse events. Network pharmacology was conducted as an exploratory analysis. After matching, measured baseline characteristics were balanced. At 1 month, the mean ODI reduction was 20.8 points with combination therapy and 14.6 points with celecoxib alone (between-group difference, -6.2 points; 95% CI, -8.36 to -4.04). Combination therapy was also associated with greater reductions in low back and leg pain and greater improvement in JOA score. Clinically meaningful ODI improvement occurred in 80.7% versus 64.0% of patients. Rescue analgesic use and treatment escalation were less frequent with combination therapy. Adverse events occurred in 19.3% and 16.0% of patients, respectively; no serious adverse events were documented. Exploratory network analyses highlighted cytokine- and inflammation-related targets and pathways. Adding Yaobitong to celecoxib may be associated with greater short-term improvement in disability, pain, and lumbar function, with no clear between-group difference in adverse events. Randomized trials with longer follow-up are warranted.

PMID 42876913
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PubMedFrontiers in pharmacology2026-10-14

Berberine and celecoxib synergistically suppress non-small cell lung cancer with EGFR/AKT/COX-2-related signaling: network pharmacology, molecular docking and experimental validation.

Wang Qiang Q, Bian Chengyu C, She Xinyuan X, Du Haonan H et al.

Non-small cell lung cancer (NSCLC) remains a major cause of cancer-related mortality, and safer combination strategies with improved antitumor efficacy are still needed. Berberine (BBR), a natural isoquinoline alkaloid with multi-target pharmacological activity, and celecoxib (CXB), a selective cyclooxygenase-2 (COX-2) inhibitor, have shown antitumor potential. However, their combined efficacy and underlying mechanisms in NSCLC remain unclear. Network pharmacology, molecular docking, Chou-Talalay combination index analysis, complementary synergy analysis using SynergyFinder+, in vitro functional assays, molecular validation, and a PC9 xenograft model were integrated to evaluate the antitumor effects and associated molecular changes of BBR combined with CXB. Candidate targets and pathways were screened using protein-protein interaction analysis, GO/KEGG enrichment, and Target-Pathway network analysis. Molecular docking was performed to assess the predicted binding affinity of BBR and CXB with key targets, and native-ligand re-docking was performed to validate the docking protocol. Cell viability, proliferation, colony formation, migration, invasion, apoptosis, and molecular changes were examined using CCK-8, EdU, colony formation, wound-healing, Transwell invasion, flow cytometry, Western blotting, qRT-PCR, immunohistochemistry, and in vivo experiments. Network analysis identified EGFR, AKT1, and PTGS2 (encoding COX-2) as candidate nodes, and molecular docking suggested predicted binding of BBR and CXB with EGFR, AKT1, and COX-2. Native-ligand re-docking showed acceptable reproduction of the crystallographic ligand poses. BBR and CXB synergistically reduced A549 and PC9 cell viability, with ZIP, HSA, Loewe, and Bliss analyses further supporting the multidose synergy, and a representative working combination dose was used for validation. The combination significantly inhibited proliferation, colony formation, migration, and invasion while promoting apoptosis. These effects were accompanied by suppression of EGFR and AKT phosphorylation, reduced COX-2 expression, downregulation of TNF-α, IL-1β, and CXCL8, decreased the Bcl-2/Bax ratio, and increased cleaved-Caspase-3. In vivo, BBR + CXB more effectively inhibited PC9 xenograft growth than either monotherapy without obvious body weight loss, accompanied by reduced Ki-67, p-EGFR, p-AKT, and COX-2 expression and increased cleaved-Caspase-3 staining. BBR combined with CXB exhibits synergistic antitumor activity in NSCLC cells and enhanced antitumor efficacy in vivo, associated with suppression of EGFR/AKT/COX-2-related signaling, attenuation of inflammatory responses, and activation of apoptosis, providing support for this potential combination strategy.

PMID 42871100
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PubMedThe AAPS journal2026-10-13

Physiologically based Biopharmaceutics Modeling (PBBM) Reveals a Low Dissolution-related Bioequivalence Risk for Immediate-Release Amlodipine Tablets.

de la Cruz Cruz Porfirio P, Gomide Larissa Lopes Rodrigues LLR, do Nascimento Gabriela Moraes GM, Urizar José Trinidad Pérez JTP et al.

A conservative BCS class III classification was recently proposed for amlodipine based on inconclusive permeability evidence. However, the scarce in vivo data suggest that amlodipine is slowly, though completely, absorbed. This means that the very rapid dissolution criterion associated with a BCS class III classification may be overly restrictive for immediate-release amlodipine products. The aim of this manuscript was to develop and validate a physiologically based biopharmaceutics model (PBBM) to assess the risk of bioequivalence failure associated with dissolution. Given that amlodipine is a lipophilic weak base, the absorption model incorporated a surrogate representation of intracellular lysosomal trapping through the FuEnt parameter, resulting in an adequate description of oral pharmacokinetics. Dissolution input included in vitro profiles obtained in phosphate buffer pH 6.8 at 50 rpm for different multisource products, fitted to either the Johnson model or the Z-factor approach. Although several products did not meet biowaiver dissolution criteria, virtual bioequivalence simulations conducted with the validated PBBM consistently predicted bioequivalence across tested formulations. Overall, these findings suggest that dissolution differences would have limited impact on the in vivo performance of amlodipine and support a low dissolution-related bioequivalence risk for immediate-release amlodipine tablets.

PMID 42864569
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PubMedInternational journal of pediatric otorhinolaryngology2026-10-13

Celecoxib as a non-inferior alternative to ibuprofen in post-tonsillectomy pain and bleeding control.

Maulsby Lexy L, Phillips Mitchell M, Evans Adele A

Post-tonsillectomy pain represents the major morbidity of the procedure, contributing to poor oral intake, dehydration, and hemorrhage. Ibuprofen, a non-selective cyclooxygenase (COX) inhibitor, is commonly used for post-operative analgesia but demonstrates potent platelet inhibition. Celecoxib, a selective COX-2 inhibitor, preserves platelet function while providing anti-inflammatory and analgesic effects. Pediatric use remains limited. To evaluate celecoxib postoperative outcomes as comparable to ibuprofen regarding pain, dehydration, and hemorrhage in pediatric tonsillectomy patients. An IRB-approved retrospective cohort study of tonsillectomies performed between January 1 to December 31, 2024 and treated with ibuprofen or celecoxib. Patients ≤18 years old who underwent tonsillectomy were identified using CPT® codes 42820, 42821, 42825, and 42826. Exclusion criteria included prior tonsillar surgery, concomitant procedures other than adenoidectomy, bleeding disorders, and opioid or alternative NSAID use. Patients were grouped by immediate post-operative analgesic regimen: celecoxib or ibuprofen. Outcomes included postoperative pain, dehydration, hemorrhage, and reoperation for bleeding. A total of 1144 patients were included (celecoxib N = 157, ibuprofen N = 987). Overall complication rates were 3.2% in the celecoxib group and 7.1% in the ibuprofen group. No statistically significant differences were observed in pain (RR, 0.27; 95% CI, 0.04-2.01), dehydration (RR, 1.72; 95% CI, 0.48-6.08), hemorrhage (RR, 0.30; 95% CI, 0.07-1.22), or return to the operating room (RR, 0.35; 95% CI, 0.05-2.60). Celecoxib demonstrated post-operative safety outcomes comparable to ibuprofen. Some parents noted practical benefits. It may represent a safe non-opioid alternative for pediatric tonsillectomy pain management.

PMID 42868944
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PubMedACS applied materials & interfaces2026-10-13

Oxygen-Amplified Carrier-Free Nanomedicine Integrating Ferroptosis/Photodynamic Therapy and COX-2/PGE2 Blockade for Robust Antitumor Immunity Against Glioma.

Huang Yinxing Y, Liu Bin B, Pan Zhenhong Z, Huang Kaikai K et al.

The therapeutic efficacy of glioma immunotherapy is severely hampered by immunosuppression in the tumor microenvironment. Here, we develop an oxygen‑amplified carrier‑free nanomedicine (IHC NPs) through hydrophobic self‑assembly of IR-820, hemin, and celecoxib. IHC NPs exhibit excellent stability, biological safety, and preferential tumor accumulation. In the subcutaneous glioma model, the combination of IHC NPs and αPD-L1 significantly inhibited subcutaneous tumor growth and effectively prevented distant tumor metastasis. Mechanistically, hemin catalyzes endogenous H2O2 to generate oxygen, thereby alleviating tumor hypoxia. This oxygen boost potentiates IR-820‑mediated photodynamic therapy and hemin-based ferroptosis, enhancing direct tumor cell killing. Concurrently, celecoxib blocks the COX‑2/PGE2 pathway, reversing immunosuppression within the tumor microenvironment. Through the synergistic strategy combining oxygen-sensitized photodynamic therapy, ferroptosis, COX-2/PGE2 suppression, and PD-1/PD-L1 blockade, this therapeutic regimen effectively induces tumor immunogenic cell death, promotes dendritic cell maturation, enhances intratumoral infiltration of cytotoxic T lymphocytes, reduces the abundance of regulatory T cells, and triggers the generation of effector memory T cells, thereby potently activating the host immune system. Collectively, our work provides a promising oxygen‑amplified carrier‑free nanomedicine for robust glioma immunotherapy.

PMID 42865137
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PubMedSkeletal radiology2026-10-13

A case report of pediatric Gardner syndrome and literature review.

Liu Meitao M, He Siping S

This case report discusses the diagnosis and treatment of a 14-year-8-month-old male patient genetically diagnosed with Gardner syndrome (GS), systematically reviewing the disease's epidemiology, clinical manifestations, imaging advances, and management strategies. The patient presented with a post-influenza A chest wall mass and had prior resections of abdominal/scalp masses. Colonoscopy revealed > 20 adenomatous polyps. Imaging demonstrated multiple craniofacial osteomas and epidermoid cysts. Genetic testing identified a pathogenic APC gene mutation (NM_000038.6:c.4669_4670del (p.Ile1557*) heterozygous variant). GS, a familial adenomatous polyposis (FAP) subtype, has an estimated pediatric incidence of 1/8000-1/14,000. Its classic triad comprises colorectal polyps, osteomas, and soft tissue tumors. Recent studies indicate earlier malignant transformation of duodenal polyps in children versus adults, with desmoid tumor incidence reaching 10-20%. In imaging, low-dose CT, panoramic radiography, and contrast-enhanced MRI can improve early detection of bone lesions and soft tissue tumors. Genetic testing (APC/MUTYH) is the pediatric screening gold standard. Optimized chemoprevention (sulindac/celecoxib) and endoscopic monitoring have significantly improved prognoses. This case highlights the urgency of multidisciplinary management and genetic counseling for pediatric GS.

PMID 42867685
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