RecruitingPhase 2NCT04924075
Endocrine
Multiple Endocrine Neoplasia Type 2
Also known as MEN2, MEN2A, MEN2B, Sipple syndrome
Multiple Endocrine Neoplasia Type 2 is an autosomal dominant syndrome caused by activating mutations in the RET proto-oncogene, subdivided into MEN2A (medullary thyroid carcinoma, pheochromocytoma, and primary hyperparathyroidism), MEN2B (m
ORPHA:653 ↗Gene RETPrevalence 1 per 35,000Onset Variable; medullary thyroid carcinoma can occur in infancy (MEN2B) to adulthoodAutosomal dominant
19
studies recruiting now
as of 7 Sept 2026
129
studies registered in total
as of 7 Sept 2026
25
countries with a recruiting site
as of 7 Sept 2026
25 Mar 2026
most recent study posted
among recruiting studies
Recruiting trials
RecruitingNCT01660984
Natural History Study of Children and Adults With Medullary Thyroid Cancer
RecruitingPhase 2NCT07492680
A Study of BMS-986504 Monotherapy and in Combination With Other Agents in Participants With Advanced and/or Metastatic Solid Tumors With Homozygous MTAP Deletion (MountainTAP-5)
RecruitingPhase 2NCT07285044
The Cancer Connected Access and Remote Expertise Beyond Walls Program to Provide In-Home Cancer Treatment and Improve Treatment Satisfaction in Cancer Patients Living in the Florida Panhandle and Surrounding Areas
RecruitingPhase 2NCT07303894
A Study of Isoquercetin in People With Ovarian Cancer
Showing the 5 most recently updated recruiting studies, as recorded 7 Sept 2026. Live status on each study page.
See all 19 recruiting studiesWhere recruiting studies are running
Countries with at least one recruiting site among the studies above, 7 Sept 2026. Tap a country to search trials there.
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About Multiple Endocrine Neoplasia Type 2
Multiple Endocrine Neoplasia Type 2 is an autosomal dominant syndrome caused by activating mutations in the RET proto-oncogene, subdivided into MEN2A (medullary thyroid carcinoma, pheochromocytoma, and primary hyperparathyroidism), MEN2B (medullary thyroid carcinoma, pheochromocytoma, mucosal neuromas, and marfanoid habitus without hyperparathyroidism), and familial medullary thyroid carcinoma. Medullary thyroid carcinoma, arising from calcitonin-secreting parafollicular C-cells, is the most penetrant and life-threatening component, with virtually 100% penetrance in RET mutation carriers, and prophylactic thyroidectomy is recommended at an age determined by the specific RET codon mutation. The genotype-phenotype correlation for RET mutations is among the best characterised in clinical genetics.
Common clinical features
Medullary thyroid carcinoma (elevated calcitonin and CEA)Neck mass or thyroid nodule on examination or ultrasoundPheochromocytoma causing hypertension and adrenergic symptomsPrimary hyperparathyroidism with hypercalcaemia (MEN2A)Mucosal neuromas of the lips, tongue, and conjunctiva (MEN2B)Marfanoid body habitus (MEN2B)Intestinal ganglioneuromatosis causing constipation (MEN2B)Diarrhoea due to calcitonin or VIP secretion from MTC
From Orphanet’s phenotype annotations (CC BY 4.0). Not a complete list.
Before you apply
Things trial teams commonly ask about for Multiple Endocrine Neoplasia Type 2. Not eligibility rules; those are set by each study.
- Identification of the specific RET codon mutation is essential; trials targeting RET kinase inhibitors require documented RET variant with known risk classification (moderate, high, or highest risk).
- Exclude active phaeochromocytoma biochemically before enrolment in any surgical or systemic therapy trial, as unresected phaeochromocytoma is an absolute contraindication to many interventions.
- Calcitonin and CEA doubling times are used as prognostic and eligibility criteria in MTC-focused trials; longitudinal serial measurements are more informative than single values.
Related conditions
Information, not medical advice. Trial listings are shown as recorded on ClinicalTrials.gov; whether any study is right for you is a decision for you and your clinicians, and eligibility is decided by each research team. Disease information from Orphanet (CC BY 4.0).