How do we know Evenity won’t have the same rebound issue as Prolia?

I've been trying to understand how Evenity works so that I can compare it to other OP drugs that have an anti-resorpative effect. Here's what I learned to the best of my understanding:

The rebound and the degree to which it happens depends on the drug's anti-resorpative mechanism. Bisphosphonates, Prolia, and Evenity impact osteoclasts in different ways and at different points in their development.

Bisphosphonates kill osteoclasts. These drugs have a long half life, so your bone turnover gradually returns to normal as the bisphosphonates wear off.

Prolia suppresses the osteoclasts by turning them into osteomorphs rendering them inactive, though they are still there, and continue being created and accumulating while you're on the drug. When you stop the drug, they fire up again . The longer you're on the drug, the more they accumulate. When you stop Prolia, as it wears off, the osteomorphs turn into osteoclasts. You have more of them than you normally would, and the rate of bone loss is accelerated.

Evenity inhibits osteoclast formation. Because the drug is so new, there isn't much information that I could find regarding what happens when the treatment ends. To the best of my understanding, the number of new osteoclasts being formed during treatment is greatly reduced. It stands to reason that there aren't huge numbers of them laying in wait like there are with Prolia. Still, I can't find anything that explains whether or not the formation of them accelerates or just returns to your "normal" rate when the treatment ends, and the drug wears off. Evenity is also anabolic, and bone growth slows down again after use, so this clearly impacts things too.

If anyone else knows where to find information about what happens physiologically in regards to osteoclast formation when you stop taking Evenity, please share.

I've been trying to understand how Evenity works so that I can compare it to other OP drugs that have an anti-resorpative effect. Here's what I learned to the best of my understanding:

The rebound and the degree to which it happens depends on the drug's anti-resorpative mechanism. Bisphosphonates, Prolia, and Evenity impact osteoclasts in different ways and at different points in their development.

Bisphosphonates kill osteoclasts. These drugs have a long half life, so your bone turnover gradually returns to normal as the bisphosphonates wear off.

Prolia suppresses the osteoclasts by turning them into osteomorphs rendering them inactive, though they are still there, and continue being created and accumulating while you're on the drug. When you stop the drug, they fire up again . The longer you're on the drug, the more they accumulate. When you stop Prolia, as it wears off, the osteomorphs turn into osteoclasts. You have more of them than you normally would, and the rate of bone loss is accelerated.

Evenity inhibits osteoclast formation. Because the drug is so new, there isn't much information that I could find regarding what happens when the treatment ends. To the best of my understanding, the number of new osteoclasts being formed during treatment is greatly reduced. It stands to reason that there aren't huge numbers of them laying in wait like there are with Prolia. Still, I can't find anything that explains whether or not the formation of them accelerates or just returns to your "normal" rate when the treatment ends, and the drug wears off. Evenity is also anabolic, and bone growth slows down again after use, so this clearly impacts things too.

If anyone else knows where to find information about what happens physiologically in regards to osteoclast formation when you stop taking Evenity, please share.