Citations

AbstractWound biofilms must be identified to target disruption and bacterial eradication but are challenging to detect with standard clinical assessment. This study tested whether bacterial fluorescence imaging could detect porphyrin‐producing bacteria within a biofilm using well‐established in vivo models. Mouse wounds were inoculated on Day 0 with planktonic bacteria (n = 39, porphyrin‐producing and non‐porphyrin‐producing species, 107 colony forming units (CFU)/wound) or with polymicrobial biofilms (n = 16, 3 biofilms per mouse, each with 1:1:1 parts Staphylococcus aureus/Escherichia coli/Enterobacter cloacae, 107 CFU/biofilm) that were grown in vitro. Mouse wounds inoculated with biofilm underwent fluorescence imaging up to Day 4 or 5. Wounds were then excised and sent for microbiological analysis. Bacteria‐matrix interaction was assessed with scanning electron microscopy (SEM) and histopathology. A total of 48 hours after inoculation with planktonic bacteria or biofilm, red fluorescence was readily detected in wounds; red fluorescence intensified up to Day 4. Red fluorescence from biofilms persisted in excised wound tissue post‐wash. SEM and histopathology confirmed bacteria‐matrix interaction. This pre‐clinical study is the first to demonstrate the fluorescence detection of bacterial biofilm in vivo using a point‐of‐care wound imaging device. These findings have implications for clinicians targeting biofilm and may facilitate improved visualisation and removal of biofilms.

Background: Light chain (AL) amyloidosis is a rare disease in which deposits of insoluble amyloid derived from immunoglobulin light chains accumulate and cause dysfunction of organs including the heart and kidneys. In order to reverse organ damage and improve overall survival, treatment must provide rapid, deep, and sustained hematologic responses. Although therapies approved for the treatment of multiple myeloma have demonstrated some efficacy, there are currently no health authority-approved treatments for AL amyloidosis. A retrospective observational study was undertaken to characterize patients and describe treatment patterns in patients with AL amyloidosis from real-world data in the US. Methods: Data were extracted from Optum Electronic Health Records (EHR) and Optum Clinformatics Data Mart (claims) databases. Eligible patients had (1) a diagnosis of AL amyloidosis (ICD-10 code E85.81) on or after January 1, 2008 or (2) a diagnosis of amyloidosis (ICD-9 codes 277.30, 277.39; ICD-10 codes E85.89, E85.9) on or after January 1, 2008 and at least one line of therapy (LOT) comprising one or more of the following treatments: bendamustine bortezomib, carfilzomib, cyclophosphamide, daratumumab, dexamethasone, doxorubicin, elotuzumab, etoposide, interferon alfa-2a, interferon alfa-2b, ixazomib, lenalidomide, melphalan, panobinostat, pomalidomide, prednisone/prednisolone, thalidomide, vincristine, or autologous stem cell transplant. Patients were required to have continuous medical enrollment during the 365 days prior to the index amyloidosis diagnosis date (claims data) or have first active date at least 365 days prior to index amyloidosis date (EHR data), must not have had prior cancer in the 365-day period prior to the index amyloidosis diagnosis date, and must have been age ≥18 years at time of amyloidosis diagnosis. Patients treated with dexamethasone only or dexamethasone and prednisolone only for ≤90 days and those treated with prednisone/prednisolone only irrespective of duration were excluded. LOTs were defined by a start date, an end date, and a distinct regimen made up of ≥1 drugs. Patients may have multiple sequential LOTs during the available follow-up period. Comorbidities were scored according to the Charlson Comorbidity Index (CCI). A score of 0 reflects no comorbidities; higher scores reflect increased mortality risk and the maximum score is 24. Descriptive statistics are provided for patient characteristics at index diagnosis date for patients who had ≥1 LOT, distribution of regimens in each LOT, treatment attrition, and duration of treatment in each line of therapy and by regimen. Results: Data from 1688 patients (Optum claims, n=624; Optum EHR, n=1064) were included in the analysis (Figure). Median age at diagnosis was 67 years and 55.7% of patients were male. Almost 70% of patients had an index diagnosis date between 2013 and 2019. The median CCI score at index diagnosis date (based on comorbidities in the 365-day pre-index diagnosis period) was 1 and 10.9% of patients had a stem cell transplant on or after the index diagnosis date. The three most common comorbidities were hypertension (50.8%), renal failure (26.2%), and congestive heart failure (24.6%). Median follow-up period was 28 months. Treatment information for regimens used by ≥5% of patients for LOT1 is summarized in the Table. The most common treatment regimen for LOT1 was a proteasome inhibitor (PI), an alkylating agent, and a steroid (n=392, 23.2%); this combination was used for an average of 111 days. Of patients treated with this combination, the most common regimen was bortezomib, cyclophosphamide, and dexamethasone (VCd), used by 358 patients. Steroid only (dexamethasone for ≥90 days) regimens accounted for 16.4% and a PI ± steroid for 13.2% of LOT1. A limitation of the study is that assumptions were used to classify AL amyloidosis vs other types of amyloidosis. Conclusions: VCd is the most commonly used regimen in patients with newly-diagnosed AL amyloidosis. This is consistent with clinical guidelines and real world data from Europe (Palladini et al, EHA 2020), supporting this regimen as the current standard of care for treatment of patients with newly-diagnosed AL amyloidosis. Disclosures Dispenzieri: Celgene: Research Funding; Pfizer: Research Funding; Alnylam: Research Funding; Intellia: Research Funding; Janssen: Research Funding; Takeda: Research Funding. Zonder:Intellia, Amgen, Takeda, Janssen, Regeneron, Alnylam, Caelum, Oncopeptides: Consultancy; BMS, Celgene: Research Funding. Hoffman:Loxo: Current equity holder in publicly-traded company; Celgene: Honoraria, Speakers Bureau. Wong:Sanofi: Membership on an entity's Board of Directors or advisory committees; Janssen: Research Funding; Fortis: Research Funding; Roche: Research Funding; GSK: Research Funding; Amgen: Consultancy; Bristol Myers Squibb: Research Funding. Liedtke:Adaptive: Membership on an entity's Board of Directors or advisory committees; Caelum: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Janssen: Membership on an entity's Board of Directors or advisory committees; GSK: Membership on an entity's Board of Directors or advisory committees; Jazz Pharmaceuticals: Membership on an entity's Board of Directors or advisory committees; Pfizer: Honoraria. Abonour:BMS: Consultancy, Research Funding; Takeda: Consultancy; Janssen: Honoraria, Research Funding; Celgene: Consultancy. D'Souza:Amgen, Merck, TenoBio: Research Funding; Akcea, Imbrium, Janssen, Pfizer: Consultancy. Lee:Janssen: Current Employment. Nair:Janssen: Current Employment. Potluri:SmartAnalyst Inc.: Current Employment. Weiss:Janssen: Current Employment, Current equity holder in publicly-traded company. Vermeulen:Janssen: Current Employment, Current equity holder in publicly-traded company. Lam:Janssen: Current Employment. Mehra:Janssen: Current Employment.

Introduction: VRD (bortezomib, lenalidomide, dexamethasone) and VCD (bortezomib, cyclophosphamide, dexamethasone) are the two most commonly used triplet induction regimens in transplant eligible patients with multiple myeloma (MM). VCD is commonly used in patients with renal dysfunction at diagnosis. Given the variable results seen in head to head comparison of these (or similar) regimens to date, no definitive conclusion can be made on whether they are equivalent. This large CIBMTR registry study compares the outcomes with VRD vs. VCD induction therapy in patients undergoing upfront autologous stem cell transplant (ASCT). Methods: Patients were included if they underwent upfront ASCT for MM from January 2013 to December 2018 within 6 months of diagnosis, received VRD or VCD induction therapy and achieved at least a partial response pre-transplant. Of 1,135 patients, 914 patients received VRD and 221 received VCD therapy. Cox proportional hazards models were created for progression-free survival (PFS) and overall survival (OS). The following covariates were adjusted in the models: induction regimen (main effect), age, sex, race, performance score, hematopoietic cell transplant-comorbidity index (HCT-CI), estimated glomerular filtration rate (eGFR) at diagnosis, immunoglobulin subtype, cytogenetics, ISS stage, response status at transplant, melphalan dose, and maintenance therapy. Results: As shown in Table 1, patients in the VRD and VCD cohorts had similar age at transplant, adjusted HCT-CI scores, and distribution of high-risk cytogenetics. Patients in the VCD group were more likely to have renal impairment and ISS stage III disease. An eGFR (mL/min/1.73m2) at diagnosis < 60 was seen in 26% of VRD patients vs. 48% of VCD patients. ISS stage III was seen in 17% vs. 34% of patients, respectively. Treatment and Response: Pre-transplant response in the VRD cohort was: complete response (CR)- 17%, very good partial response (VGPR)- 48% and partial response (PR)- 35%. Response in the VCD cohort was: CR- 17%, VGPR- 42% and PR- 41%. Conditioning dose was melphalan 200 mg/m2 in 80% of patients receiving VRD vs. 69% in the VCD group. Post-transplant response was at least VGPR in 74% vs. 75% of patients, respectively. Maintenance in the VRD group was: lenalidomide based (+/- bortezomib)- 80%, bortezomib based- 5%, other-3% and none- 12% of patients. In the VCD group, maintenance was: lenalidomide based- 63%, bortezomib based- 11%, other- 1% and none- 24%. Survival: Patients receiving VRD induction had superior outcomes compared to VCD induction with median PFS from transplant of 44.6 (38.0-55.8) months vs 34.1 (25.8-44.7) months, p 0.004 respectively. Median OS was not reached for either group, with 5-year OS 79 (74-83)% for VRD and 60 (50-69)% for VCD, p <0.001. Univariate PFS and OS outcomes by induction regimen and eGFR at diagnosis are shown in Table 2 and Figure 1. Multivariate analysis is shown in Table 3. After adjusting for prognostic factors, there was no statistically significant difference between the two induction regimens, with hazard ratio (HR) for PFS in the VCD vs VRD group being 1.22 (95% CI: 0.96-1.55, p=0.10). ISS stage, cytogenetics, disease status prior to transplant, and maintenance were independent prognostic factors for PFS. Similarly, on multivariate analysis for OS, there was no statistically significant difference in the two groups, with HR for OS in VCD vs VRD group being 1.33 (95% CI: 0.93-1.92, p=0.12). ISS stage, cytogenetics, disease status prior to transplant, and maintenance were independent prognostic factors for OS. Conclusions: In patients with MM undergoing upfront transplant after VRD or VCD induction, no difference in outcomes was seen based on the induction therapy received after adjusting for other prognostic factors. As several MM patients with renal dysfunction are started on VCD, it is reassuring to see that VCD was not associated with inferior PFS, likely due to the eventual transition to maintenance therapy in the majority due to subsequent improvement of renal function. The use of maintenance treatment was uniformly associated with superior outcomes. Disclosures Sidana: Janssen: Consultancy. Kumar:Oncopeptides: Consultancy, Other: Independent Review Committee; IRC member; Kite Pharma: Consultancy, Research Funding; Genentech/Roche: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Celgene/BMS: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Dr. Reddy's Laboratories: Honoraria; Amgen: Consultancy, Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments, Research Funding; Janssen Oncology: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Takeda: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; AbbVie: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Novartis: Research Funding; Sanofi: Research Funding; MedImmune: Research Funding; Karyopharm: Consultancy; BMS: Consultancy, Research Funding; Tenebio: Other, Research Funding; Genecentrix: Consultancy; Carsgen: Other, Research Funding; Cellectar: Other; Merck: Consultancy, Research Funding; Adaptive Biotechnologies: Consultancy. Giralt:Johnson & Johnson: Membership on an entity's Board of Directors or advisory committees, Research Funding; Celgene: Membership on an entity's Board of Directors or advisory committees, Research Funding; Actinuum: Other: Advisory board, Research Funding; Amgen: Other: Advisory Board, Research Funding; KITE: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees; OMEROS: Research Funding; SPECTRUM Pharma: Membership on an entity's Board of Directors or advisory committees; BMS: Membership on an entity's Board of Directors or advisory committees, Research Funding; Sanofi: Membership on an entity's Board of Directors or advisory committees, Research Funding; GSK: Membership on an entity's Board of Directors or advisory committees, Research Funding; PFIZER: Membership on an entity's Board of Directors or advisory committees, Research Funding; Jensenn: Membership on an entity's Board of Directors or advisory committees, Research Funding; TAKEDA: Membership on an entity's Board of Directors or advisory committees, Research Funding; MILTENYI: Research Funding; JAZZ Pharmaceutical: Membership on an entity's Board of Directors or advisory committees. Qazilbash:Janssen: Research Funding; Bioclinica: Consultancy; Amgen: Research Funding; Angiocrine: Research Funding; Bioline: Research Funding. Shah:GSK, Amgen, Indapta Therapeutics, Sanofi, BMS, CareDx, Kite, Karyopharm: Consultancy; BMS, Janssen, Bluebird Bio, Sutro Biopharma, Teneobio, Poseida, Nektar: Research Funding. D'Souza:Janssen: Consultancy; Akcea: Consultancy; Imbrium: Consultancy; Merck: Research Funding; Pfizer: Consultancy; Teneobio: Research Funding; Amgen: Research Funding.

AbstractObjectiveWe quantified the representation of female program directors (PDs) and assessed their respective demographics, academic metrics, and program-related characteristics in chronic pain and acute pain medicine fellowship programs accredited by the Accreditation Council for Graduate Medical Education (ACGME).MethodsWe identified chronic and acute pain PDs on the ACGME website on November 15, 2020. We abstracted data from public databases and performed comparisons of demographics, academic metrics, and program-related characteristics between female and male PDs.ResultsWe identified 111 chronic pain programs and 35 acute pain programs. Overall, there were 35 (31.5%) chronic pain programs with a female PD and 76 (68.5%) chronic pain programs with a male PD. Female chronic pain PDs published fewer peer-reviewed articles (4.0 publications, interquartile range [IQR] = 2.0–12.0) compared with male chronic pain PDs (9.0 publications, IQR = 4.0–27.0; P = 0.050), although there was no difference in the H-index score (3.0 vs 4.0 publications, respectively; P = 0.062) or senior academic rank status (57.1% vs 50.0%, respectively; P = 0.543). There were 10 (28.6%) acute pain programs with a female PD and 25 (71.4%) acute pain programs with a male PD. Similar to the chronic pain cohort, there was no difference in senior academic rank status based on gender in acute pain PDs (50.0% vs 24.0%, respectively; P = 0.227).ConclusionOur study highlights gender differences in the PD role in ACGME-accredited chronic and acute pain fellowships. Female PDs remain underrepresented and have fewer peer-reviewed publications. Senior academic rank status was similar across genders, contradicting the current evidence in academic medicine.

ABSTRACT Background Since the Accreditation Council for Graduate Medical Education (ACGME) established the designated institutional official (DIO) role in 1998, there have been major changes in sponsoring institutions (SIs) and DIO responsibilities. Yet there remains a large gap in our knowledge regarding baseline SI and DIO characteristics as well as a need for institutions wanting to increase diversity in the DIO role and other leadership positions within the medical education community. Objective We sought to characterize demographics of DIOs and the SIs they oversee. Methods We identified SIs and DIOs on the ACGME website on February 15, 2020. Reviewed data included SI accreditation status, number of programs and resident/fellow positions, and DIO characteristics. Results We identified 831 SIs. SIs with continued accreditation sponsored more programs (median 4.0) than SIs with initial accreditation (median 1.0, P < .001). DIO age ranged from 29–81 years (median 57 years). Two-hundred eighty-three of 831 (34%) DIOs were women. Of 576 DIOs with known academic rank, 356 (62%) DIOs held senior academic rank. A higher proportion of male DIOs had senior academic rank (68% vs 52%; OR 1.90 [95% CI 1.34–2.70]; P < .001) and professor rank (39% vs 24%; OR 2.01 [95% CI 1.38–2.94]; P < .001) compared to female DIOs. Female gender was associated with a greater number of ACGME-accredited programs and filled resident/fellow positions per SI (P < .001 for both). Conclusions This study describes characteristics of DIOs and SIs and offers insights for those pursuing a DIO position.

Abstract Despite substantial advances in stroke care, vascular cognitive impairment remains a prominent source of disability. Unlike sensorimotor impairments, cognition often continues to decline after stroke. An aging population will increase the prevalence of vascular cognitive impairment, with stroke playing an important role. Ten percent of patients presenting with stroke have pre-stroke dementia; an additional 10% will develop incident dementia with a first stroke, and 30% with a recurrent stroke. While stroke increases the risk of cognitive impairment, the presence of cognitive impairment also impacts acute stroke treatment and increases risk of poor outcome by nearly twofold. There is substantial overlap in the clinical and pathological aspects of vascular and degenerative dementias in many patients. How they relate to one another is controversial. The treatment of vascular cognitive impairment remains supportive, focusing on treating vascular risk factors. Cognitive rehabilitation after stroke is an area of active research, and existing pharmacologic treatments have limited benefit. Heightened awareness of cognitive impairment in the setting of stroke is imperative for prognostication and management, impetus for research and, ultimately, the discovery of efficacious treatments.

Background: BCMA targeted immunotherapy has yielded promising results for relapsed/refractory multiple myeloma (RRMM). TNB-383B is a BCMA x CD3 bispecific T-cell redirecting antibody incorporating a unique anti-CD3 moiety that preferentially activates effector over regulatory T-cells and uncouples cytokine release from anti-tumor activity, as well as 2 heavy-chain-only anti-BCMA moieties for a 2:1 tumor associated antigen to CD3 stoichiometry. Results from the ongoing phase 1 dose escalation and expansion First-in-Human (FIH) study of TNB-383B are presented (NCT03933735). Methods: Eligible patients have RRMM and have been exposed to at least 3 prior lines of therapy including a proteasome inhibitor, an immunomodulatory drug, and an anti-CD38 monoclonal antibody. Patients have been treated with escalating doses of TNB-383B infused IV over 1-2 hours Q3W (without step-up dosing). The primary objectives are to determine the safety/tolerability and clinical pharmacology of TNB-383B and to identify the MTD/RP2D. The study used a 3+3 design for dose escalation, with additional patients enrolled on cleared dose levels. Patients on earlier dose cohorts were allowed to increase to the highest cleared dose with investigator consensus. Responses were assessed by IMWG criteria and Adverse Events (AEs) were graded according to CTCAE v5.0. Minimal residual disease (MRD) assessment was performed via NGS on bone marrow samples in patients achieving a complete response (CR). Results: As of 13 July 2020, 38 subjects have been dosed with TNB-383B (0.025 - 40 mg). Demographics and disease characteristics at study entry are summarized in Table 1. The most common Gr 3/4 AEs were anemia (6/38; 16%) and thrombocytopenia (5/38; 13%). The most common drug-related AEs were CRS (8/38; 21%) and headache (5/38; 13%). One case of Gr 2 CRS was observed at 0.075 mg; all other CRS events were seen at 5.4 mg and above. Cases of CRS were grade 1 (5/8) or 2 (3/8) and occurred only after the first dose of TNB-383B. All but 3 subjects were managed with fluids and acetaminophen (the other 3 received 1 dose each of tocilizumab). One DLT, Gr3 confusion that resolved within 6 hours without sequelae was seen at the 20 mg dose in an additional patient enrolled on this cohort. No IRRs were observed. Dose modification was necessary in 1 subject for Gr 3 neutropenia associated with CRS; the subject escalated to their full dose after tolerating subsequent doses without incident. 5 subjects died from their underlying disease during follow-up. 15 subjects discontinued treatment, all of them for progressive disease. Preliminary PK data support Q3W dosing of TNB-383B. Activity was observed in one patient each at 0.2 mg and 1.8 mg; at doses of 5.4 - 40 mg an ORR of 52% (12/23) was observed. Depth and duration of response are summarized in Table 2. Conclusions: TNB-383B is well tolerated at doses up to 40 mg, without the need for step/split dosing. A preliminary ORR of 52% (12/23) was observed at doses ≥ 5.4 mg, including deep (6 PR / 3 VGPR / 3 CR) and durable (up to 24 weeks) responses despite dosing only every 3 weeks. Enrollment into the dose escalation arm is ongoing; updated data will be presented at the meeting. Disclosures Rodriguez: BMS, Takeda, Amgen: Consultancy, Speakers Bureau. D'Souza:Amgen: Research Funding; Akcea: Consultancy; Pfizer: Consultancy; Teneobio: Research Funding; Imbrium: Consultancy; Merck: Research Funding; Janssen: Consultancy. Shah:GSK, Amgen, Indapta Therapeutics, Sanofi, BMS, CareDx, Kite, Karyopharm: Consultancy; BMS, Janssen, Bluebird Bio, Sutro Biopharma, Teneobio, Poseida, Nektar: Research Funding. Voorhees:Bristol-Myers Squibb: Other: Personal fees; Adaptive Biotechnologies: Other: Personal fees; Novartis: Other: Personal fees; Celgene: Other: Personal fees; Janssen: Other: Personal fees; Oncopeptides: Other: Personal fees; TeneoBio: Other: Personal fees; Levine Cancer Institute, Atrium Health: Current Employment. Buelow:Teneobio, Inc.: Current Employment, Current equity holder in private company. Kumar:Karyopharm: Consultancy; Tenebio: Other, Research Funding; Sanofi: Research Funding; Oncopeptides: Consultancy, Other: Independent Review Committee; IRC member; AbbVie: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Genecentrix: Consultancy; Dr. Reddy's Laboratories: Honoraria; Adaptive Biotechnologies: Consultancy; Merck: Consultancy, Research Funding; Takeda: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; BMS: Consultancy, Research Funding; Cellectar: Other; Janssen Oncology: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Carsgen: Other, Research Funding; Amgen: Consultancy, Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments, Research Funding; Celgene/BMS: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Novartis: Research Funding; MedImmune: Research Funding; Genentech/Roche: Other: Research funding for clinical trials to the institution, Consulting/Advisory Board participation with no personal payments; Kite Pharma: Consultancy, Research Funding.

AbstractWe studied 2,528 patients with upfront autologous haematopoietic cell transplantation (AHCT) for multiple myeloma (MM) from 2008–2017 to develop a prognostic model to predict outcomes. High‐risk cytogenetics included t(4;14), t(14;16), t(14;20), del13q on karyotype, del17p, +1q or 1pdel. A Cox model identified factors prognostic of progression/relapse in a training subset (n = 1,246). A weighted score using these factors was assigned to a validation cohort (n = 774). Presence of high‐risk cytogenetics [hazard ratio, (HR) 1·68 (1·3–2·17)] and pre‐AHCT bone marrow plasma cells (BMPCs) ≥10% [1·68 (1·33–2·12)] were assigned 4 points each; albumin at diagnosis <3·5 g/dl [1·31 (1·07–1·61)] 2; standard risk cytogenetics 1, and no cytogenetics abnormality, BMPCs <10% at AHCT and albumin ≥3·5 g/dl at diagnosis 0 points each. A three‐category system with low risk (0–3), intermediate risk (4–8) and high risk (9–10) showed 3‐year progression‐free survival in the low vs. intermediate vs. high risk of 58% (95% CI: 52–63) vs. 49% (95% CI: 43–56) vs. 31% (95% CI: 12–51), P < 0.001 respectively, and 3‐year OS in low vs. intermediate vs. high risk of 88% (95% CI: 84–91) vs. 81% (95% CI: 76–86) vs. 64% (95% CI: 39–80); P < 0·001. Our prognostic scoring system can identify MM patients at risk for early relapse after AHCT.

AbstractBackgroundThe gut is the only organ system with intrinsic neural reflexes. Intrinsic primary afferent neurons (IPANs) of the enteric nervous system initiate intrinsic reflexes, form gut‐brain connections, and undergo considerable neuroplasticity to cause digestive diseases. They remain inaccessible to study in mice in the absence of a selective marker. Advillin is used as a marker for primary afferent neurons in dorsal root ganglia. The aim of this study was to test the hypothesis that advillin is expressed in IPANs of the mouse jejunum.MethodsAdvillin expression was assessed with immunohistochemistry and using transgenic mice expressing an inducible Cre recombinase under the advillin promoter were used to drive tdTomato and the genetically encoded calcium indicator GCaMP5. These mice were used to characterize the morphology and physiology of advillin‐expressing enteric neurons using confocal microscopy, calcium imaging, and whole‐cell patch‐clamp electrophysiology.Key ResultsAdvillin is expressed in about 25% of myenteric neurons of the mouse jejunum, and these neurons demonstrate the requisite properties of IPANs. Functionally, they demonstrate calcium responses following mechanical stimuli of the mucosa and during antidromic action potentials. They have Dogiel type II morphology with neural processes that mostly remain within the myenteric plexus, but also project to the mucosa and express NeuN and calcitonin gene‐related peptide (CGRP), but not nNOS.Conclusions and InferencesAdvillin marks jejunal IPANs providing accessibility to this important neuronal population to study and model digestive disease.