Please tell us about your clinical practice, background in treating IBS-C and research in the space. How many patients do you treat, and what is your preferred first-line therapy?

How much of a need for a new treatment is there in this space?

How does tenapanor’s inhibition of the sodium transporter NHE3 mechanism of action work to reduce sodium uptake from the gut, and why is that important in IBS-C?

How efficient are Efgartigimod/ SYNT001/ PRN10008 at binding FcRn and blocking IgG recycling/ increasing IgG clearance vs its competition?

What’s your take on the compliance rate of tenapanor in the t3 long term trial at 98%,the 2.1% discontinuation rate, (of which 1.7% due to diarrhea), and the most common adverse event being diarrhea at 9.2%. Is it high/low, vs other trials you’ve seen in IBS-C?

An older trial from 2017 reported greater than placebo rates for diarrhea (16.0% vs. 3.7%), flatulence (3.1% vs. 1.0%), nasopharyngitis (4.4% vs. 3.7%) and abdominal distension (3.4% vs. 0.3%). The placebo adjusted discontinuation rate due to diarrhea was 5.8 percent. What could account for the differences in that trial vs the long term safety trial?

In a phase 3 multicenter U.S. trial with 593 patients, data showed the combined response consisting of at least a 30% drop from baseline in reported abdominal pain and an increase of at least one complete spontaneous bowel movement per week for 6 of the first 12 weeks of treatment. This combined response occurred in 37% of patients treated with tenapanor at a dosage of 50 mg oral, compared with a 24% rate among the placebo-control patients. What’s the significance/impact of this data?

Any comments on the pill burden of tenapanor vs other oral treatments? Is the dose significantly lower with tenapanor?