35 replies to this topic

[mag1]

NKTR214!!!

It's time for everyone to party!

Unreal!

Edited by mag1, 14 November 2017 - 06:59 AM.

[jondoeuk]

NKTR214!!!

It's time for everyone to party!

Unreal!

 

One of the highlights from the whole conference. I can't wait to see how the data matures.

[mag1]

The funny thing was CALA's stock price collapsed and no one could figure out why.

It really does not make much sense.

CB839 came in pretty much on target, though NKTR just posted overwhelmingly positive results.

 

If a patient did not respond to NKTR214, could always rotate to CB839!

Would seem like a great combo.

CB839 shows responses typically within a month which can be predicted by inflammation gene screening. 

[jondoeuk]

The funny thing was CALA's stock price collapsed and no one could figure out why.

It really does not make much sense.

CB839 came in pretty much on target, though NKTR just posted overwhelmingly positive results.

 

If a patient did not respond to NKTR214, could always rotate to CB839!

Would seem like a great combo.

CB839 shows responses typically within a month which can be predicted by inflammation gene screening. 

I assume (rightly or wrongly) that a people were trying to make direct comparisons between the trials despite the fact both had completely different patient populations and the two compounds had different MOAs. I agree that it would be nice to see a combo trial as they could have additive or synergistic effects.

[jondoeuk]

A Single Direct Intratumoral Injection of TTI-621 (SIRPaFc) Induces Antitumor Activity in Patients with Relapsed/Refractory Mycosis Fungoides and Sézary Syndrome: Preliminary Findings Employing an Immune Checkpoint Inhibitor Blocking the CD47 “Do Not Eat” Signal http://s2.q4cdn.com/...-4076-FINAL.pdf

 

This poster highlighted preliminary safety and antitumour activity of intratumoral TTI-621 administration in highly pretreated patients with relapsed or refractory mycosis fungoides or Sézary syndrome. Intratumoral injection was well tolerated, with no dose-limiting toxicity observed. A rapid reduction in CAILS scores, which measures local lesion responses, was observed in 9 out of 10 mycosis fungoides patients and a reduction in circulating leukemic Sézary cells was observed in 3 out of 3 patients. Several patient profiles were presented which demonstrate clinical responses in disfiguring lesions, in some cases after a single dose of TTI-621. Collectively, the data demonstrate that cutaneous T-cell lymphoma (CTCL) appears biologically responsive to intratumoral injections of TTI-621.

 

TTI-621 (SIRPaFc), an Immune Checkpoint Inhibitor Blocking the CD47 “Do Not Eat” Signal, Induces Objective Responses in Patients with Advanced, Relapsed/Refractory Diffuse Large B-cell Lymphoma (DLBCL) http://s2.q4cdn.com/...-4116-FINAL.pdf

 

This presentation summarised the overall safety profile of intravenous TTI-621 in patients with relapsed/refractory hematologic malignancies and preliminary antitumour activity in patients with diffuse large B-cell lymphoma (DLBCL). Weekly infusions of TTI-621 were shown to be well tolerated, and notably, transient thrombocytopenia was attenuated after the first dose. These data, combined with the previously reported results from the dose escalation phase, demonstrate a favourable safety profile of intravenous TTI-621 in over 100 patients. Intravenous administration of TTI-621, particularly in combination with Rituximab, resulted in objective responses in 5 out of 18 evaluable patients with heavily pre-treated, relapsed/refractory DLBCL, and several others experienced prolonged progression-free intervals.

[mag1]

jon, might you comment on how chronobiology might be combined with glycolysis inhibitors?

 

A simple intervention of housing mice in a blue tinted box versus clear box changed melatonin

levels (circadian pathway) which resulted in marked delay in tumor growth (PMID:26678364).

 

Dexamethasone injections and heat shock in a melanoma model also delayed tumor growth

(PMID:28196531).

 

Might you have any general suggestions of how glycolysis inhibitors (e.g. 3-BP) might be made

more powerful by using a circadian strategy? For example, would targeting cancer cells with an

anti-glycolytic during the night be especially helpful as normal cells would be in a reduced metabolic

state while cancer cells would still be in an active state?